@article{sannes_2017, title={Hyaluronan: Local Climate Change in Asthma?}, volume={57}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2017-0276ed}, abstractNote={The extracellular matrix (ECM) in the lung is most commonly characterized in terms of its fundamental fibrillar composition: type I collagen and elastic fibers. These elegant structural proteins give the lungs their remarkable physiologic characteristics that have provided selective advantages for vertebrate life forms, and their study has provided gainful employment for research and clinical professionals who deal with their involvement in a variety of diseases. Their functional impacts are readily measurable, and highly useful for defining normal versus abnormal health status. A fuller understanding of other components of the ECM’s composition and functionality has finally begun to emerge, and with it has come an appreciation for the complex intricacies of their contributions to biological microenvironments and relationships with cells, both fixed and migratory. Clearly, what can be physically and microscopically visualized and quantified has commanded the attention of basic and clinical scientists alike, and rightfully so. Much of what goes wrong in the lung ultimately affects collagen and elastic fiber integrity and function, as manifested in chronic obstructive pulmonary disease, interstitial lung disease, bronchopulmonary displasia, and related diseases. The significant quantities of so-called “ground substance,” which includes the glycosaminoglycans chondroitin sulfate, dermatan sulfate, keratan sulfate, heparan sulfate, heparin, and hyaluronan (HA; also known as hyaluronate or hyaluronic acid), were presumed to function primarily to hold water and thought of simply as an interstitial filler, adding volume and texture. Early work on tissue regeneration, however, demonstrated that this “filler” could be very important biologically. Studies in newt limbs were the first to show that proliferation occurred in HA-rich tissues, and differentiation was closely linked with chondroitin sulfate (1). These and numerous subsequent studies led to the conclusion that the production or removal of specific nonfibrillar ECM components necessarily preceded temporally organized, critical events that control cellular attachment, migration, differentiation, survival, and/or senescence, as well as tissue expansion and maturation. Importantly, this conceptually changed how ECMs fit into the context of the biological activities of a tissue and/or organ, and codified them as true biological response modifiers. HA has been studied in a wide variety of biological systems and pathologies. It is a critical regulator of inflammation (2) and has a distinct role in airway diseases such as rhinosinusitis, asthma, chronic obstructive pulmonary disease, cystic fibrosis, and primary ciliary dyskinesia (3, 4). More specifically, HA has been shown to orchestrate TGF-b–dependent maintenance of the myofibroblast phenotype (5) and control the deposition of fibronectin and collagen, as well as TGF-b induction of lung myofibroblasts (6). Relatedly, HA synthase 2 (HAS2), a membrane-bound enzyme that is responsible for the production of HA, regulates fibroblast senescence in pulmonary fibrosis (7). In this issue of the Journal, Walker and colleagues (pp. 702–710) hypothesize that peribronchiolar accumulation of HA contributes to airway inflammation, remodeling, and hyperresponsiveness in asthma (8). To examine its role(s) in this context, they challenged mice with targeted overexpression of HAS2 to stimulate production of HA. They then examined its overexpression in myofibroblasts and smooth muscle cells expressing the a-smooth muscle actin (a-SMA) promoter in a chronic model of allergic airway disease using aerosolized ovalbumin (OVA). Predictably, the results demonstrated significantly increased peribronchial HA in OVA-challenged a-SMA–HAS mice, with an accompanying increase in collagen (trichrome staining) compared with a-SMA– HAS and naive a-SMA–HAS mice. One of the major unexpected findings, however, was that these same animals displayed significantly reduced airway responsiveness to methacholine compared with a-SMA–HAS2 mice. This was attributed to the observed peribronchial fibrosis and resulting stiffness of the proximal airways, as evidenced by measured airway resistance. Interestingly, unchallenged a-SMA–HAS mice had peribronchial HA levels comparable to those observed in the OVA-challenged a-SMA–HAS mice, which did not correlate with a-SMA and collagen levels, suggesting that overexpression of HAS alone does not drive the tissue response. However, previous studies have shown that HA from myofibroblasts can promote collagen synthesis and deposition (9, 10), and the authors argue in favor of the notion that HAS overexpression contributes to myofibroblast and smooth muscle cell–mediated increased collagen deposition, leading to stiffer airways. This argument might have been strengthened by measurements of total lung collagen (hydroxyproline) and/or gene expression of Col1a1 and/or fibronectin (11). Nevertheless, similar increases in HA, HAS2, and HAS3 have been observed in a cockroach antigen–induced model of allergic asthma in mice, and increased expression of HAS2 and HAS3 was found in primary isolated bronchial epithelial cells from asthmatic children compared with those from healthy children (12). Collectively, this and previous studies suggest important roles for HAS expression and HA production by airway fibroblasts in tissue remodeling and alterations in airway responsiveness in allergic asthma. It is hoped that in this will define the role that HA fragments play in the described model, as they have previously been shown to be important mediators in human asthma (13). These studies provide new insights into components of the ECM as important biological response modifiers in the lung, and provide a new and expanding context for basic and clinical pulmonary research. n}, number={6}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Sannes, Philip L.}, year={2017}, month={Dec}, pages={635–636} }
 @article{newman_sills_hanrahan_ziegler_tidd_cook_sannes_2015, title={Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-β and WNT7B in Human Lung Fibroblasts}, volume={64}, ISSN={0022-1554 1551-5044}, url={http://dx.doi.org/10.1369/0022155415617988}, DOI={10.1369/0022155415617988}, abstractNote={ The wingless (Wnt) family of signaling ligands contributes significantly to lung development and is highly expressed in patients with usual interstitial pneumonia (UIP). We sought to define the cellular distribution of Wnt5A in the lung tissue of patients with idiopathic pulmonary fibrosis (IPF) and the signaling ligands that control its expression in human lung fibroblasts and IPF myofibroblasts. Tissue sections from 40 patients diagnosed with IPF or UIP were probed for the immunolocalization of Wnt5A. Further, isolated lung fibroblasts from normal or IPF human lungs, adenovirally transduced for the overexpression or silencing of Wnt7B or treated with TGF-β1 or its inhibitor, were analyzed for Wnt5A protein expression. Wnt5A was expressed in IPF lungs by airway and alveolar epithelium, smooth muscle cells, endothelium, and myofibroblasts of fibroblastic foci and throughout the interstitium. Forced overexpression of Wnt7B with or without TGF-β1 treatment significantly increased Wnt5A protein expression in normal human smooth muscle cells and fibroblasts but not in IPF myofibroblasts where Wnt5A was already highly expressed. The results demonstrate a wide distribution of Wnt5A expression in cells of the IPF lung and reveal that it is significantly increased by Wnt7B and TGF-β1, which, in combination, could represent key signaling pathways that modulate the pathogenesis of IPF. }, number={2}, journal={Journal of Histochemistry & Cytochemistry}, publisher={SAGE Publications}, author={Newman, Donna R. and Sills, W. Shane and Hanrahan, Katherine and Ziegler, Amanda and Tidd, Kathleen McGinnis and Cook, Elizabeth and Sannes, Philip L.}, year={2015}, month={Nov}, pages={99–111} }
 @article{yi_newman_zhang_johansson_sannes_2015, title={Heparin and LPS-induced COX-2 expression in airway cells: a link between its anti-inflammatory effects and GAG sulfation}, volume={41}, ISSN={["1521-0499"]}, DOI={10.3109/01902148.2015.1091053}, abstractNote={ABSTRACT Purpose/Aim: Previous studies have indicated that the sulfated polysaccharide heparin has anti-inflammatory effects. However, the mechanistic basis for these effects has not been fully elucidated. Materials and Methods: NCI-H292 (mucoepidermoid) and HBE-1 (normal) human bronchial epithelial cells were treated with LPS alone or in the presence of high-molecular-weight (HMW) fully sulfated heparin or desulfated HMW heparin. Cells were harvested to examine the phosphorylation levels of ERK1/2, p38, and NF-kB p65 and COX-2 protein expression by Western blot and gene expression of both COX-2 and CXCL-8 by TaqMan qRT-PCR. Results: Heparin is known to exert an influence on receptor-mediated signaling through its ability to both potentiate and inhibit the receptor-ligand interaction, depending upon its concentration. In H292 cells, fully-sulfated HMW heparin significantly reduced LPS-induced gene expression of both COX-2 and CXCL-8 for up to 48 hours, while desulfated heparin had little to no significant suppressive effect on signaling or on COX-2 gene or protein expression. Desulfated heparin, initially ineffective at preventing LPS-induced CXCL8 up-regulation, reduced CXCL8 transcription at 24 hours. In contrast, in normal HBE-1 cells, fully sulfated heparin significantly suppressed only ERK signaling, COX-2 gene expression at 12 hours, and CXCL-8 gene expression at 6 and 12 hours, while desulfated heparin had no significant effects on LPS-stimulated signaling or on gene or protein expression. Sulfation determines heparin's influence and may reflect the moderating role of GAG sulfation in lung injury and health. Conclusions: Heparin's anti-inflammatory effects result from its nonspecific suppression of signaling and gene expression and are determined by its sulfation.}, number={9}, journal={EXPERIMENTAL LUNG RESEARCH}, author={Yi, Na Young and Newman, Donna R. and Zhang, Huiying and Johansson, Helena Morales and Sannes, Philip L.}, year={2015}, month={Oct}, pages={499–513} }
 @article{muthusamy_sommerville_moeser_stumpo_sannes_adler_blackshear_weimer_ghashghaei_2015, title={MARCKS-dependent mucin clearance and lipid metabolism in ependymal cells are required for maintenance of forebrain homeostasis during aging}, volume={14}, ISSN={["1474-9726"]}, DOI={10.1111/acel.12354}, abstractNote={Summary}, number={5}, journal={AGING CELL}, author={Muthusamy, Nagendran and Sommerville, Laura J. and Moeser, Adam J. and Stumpo, Deborah J. and Sannes, Philip and Adler, Kenneth and Blackshear, Perry J. and Weimer, Jill M. and Ghashghaei, H. Troy}, year={2015}, month={Oct}, pages={764–773} }
 @article{johansson_newman_sannes_2014, title={Whole-Genome Analysis of Temporal Gene Expression during Early Transdifferentiation of Human Lung Alveolar Epithelial Type 2 Cells In Vitro}, volume={9}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0093413}, abstractNote={It is generally accepted that the surfactant-producing pulmonary alveolar epithelial type II (AT2) cell acts as the progenitor of the type I (AT1) cell, but the regulatory mechanisms involved in this relationship remain the subject of active investigation. While previous studies have established a number of specific markers that are expressed during transdifferentiation from AT2 to AT1 cells, we hypothesized that additional, previously unrecognized, signaling pathways and relevant cellular functions are transcriptionally regulated at early stages of AT2 transition. In this study, a discovery-based gene expression profile analysis was undertaken of freshly isolated human AT2 (hAT2) cells grown on extracellular matrix (ECM) substrata known to either support (type I collagen) or retard (Matrigel) the early transdifferentiation process into hAT1-like cells over the first three days. Cell type-specific expression patterns analyzed by Illumina Human HT-12 BeadChip yielded over 300 genes that were up- or down-regulated. Candidate genes significantly induced or down-regulated during hAT2 transition to hAT1-like cells compared to non-transitioning hAT2 cells were identified. Major functional groups were also recognized, including those of signaling and cytoskeletal proteins as well as genes of unknown function. Expression of established signatures of hAT2 and hAT1 cells, such as surfactant proteins, caveolin-1, and channels and transporters, was confirmed. Selected novel genes further validated by qRT-PCR, protein expression analysis, and/or cellular localization included SPOCK2, PLEKHO1, SPRED1, RAB11FIP1, PTRF/CAVIN-1 and RAP1GAP. These results further demonstrate the utility of genome-wide analysis to identify relevant, novel cell type-specific signatures of early ECM-regulated alveolar epithelial transdifferentiation processes in vitro.}, number={4}, journal={PLOS ONE}, author={Johansson, Helena Morales and Newman, Donna R. and Sannes, Philip L.}, year={2014}, month={Apr} }
 @article{coffey_newman_sannes_2013, title={Expression of Fibroblast Growth Factor 9 in Normal Human Lung and Idiopathic Pulmonary Fibrosis}, volume={61}, ISSN={["0022-1554"]}, DOI={10.1369/0022155413497366}, abstractNote={ The fibroblast growth factor (FGF) family of signaling ligands contributes significantly to lung development and maintenance in the adult. FGF9 is involved in control of epithelial branching and mesenchymal proliferation and expansion in developing lungs. However, its activity and expression in the normal adult lung and by epithelial and interstitial cells in fibroproliferative diseases like idiopathic pulmonary fibrosis (IPF) are unknown. Tissue samples from normal organ donor human lungs and those of a cohort of patients with mild to severe IPF were sectioned and stained for the immunolocalization of FGF9. In normal lungs, FGF9 was confined to smooth muscle surrounding airways, alveolar ducts and sacs, and blood vessels. In addition to these same sites, lungs of IPF patients expressed FGF9 in a population of myofibroblasts within fibroblastic foci, hypertrophic and hyperplastic epithelium of airways and alveoli, and smooth muscle cells surrounding vessels embedded in thickened interstitium. The results demonstrate that FGF9 protein increased in regions of active cellular hyperplasia, metaplasia, and fibrotic expansion of IPF lungs, and in isolated human lung fibroblasts treated with TGF-β1 and/or overexpressing Wnt7B. The cellular distribution and established biologic activity of FGF9 make it a potentially strong candidate for contributing to the progression of IPF. }, number={9}, journal={JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY}, author={Coffey, Emily and Newman, Donna R. and Sannes, Philip L.}, year={2013}, month={Sep}, pages={671–679} }
 @article{zhang_newman_sannes_2012, title={HSULF-1 inhibits ERK and AKT signaling and decreases cell viability in vitro in human lung epithelial cells}, volume={13}, ISSN={1465-9921}, url={http://dx.doi.org/10.1186/1465-9921-13-69}, DOI={10.1186/1465-9921-13-69}, abstractNote={Abstract}, number={1}, journal={Respiratory Research}, publisher={Springer Nature}, author={Zhang, Huiying and Newman, Donna R and Sannes, Philip L}, year={2012}, pages={69} }
 @article{zhang_newman_bonner_sannes_2012, title={Over-expression of human endosulfatase-1 exacerbates cadmium-induced injury to transformed human lung cells in vitro}, volume={265}, ISSN={["1096-0333"]}, DOI={10.1016/j.taap.2012.09.008}, abstractNote={Environmental exposure to cadmium is known to cause damage to alveolar epithelial cells of the lung, impair their capacity to repair, and result in permanent structural alterations. Cell surface heparan sulfate proteoglycans (HSPGs) can modulate cell responses to injury through their interactions with soluble effector molecules. These interactions are often sulfate specific, and the removal of sulfate groups from HS side chains could be expected to influence cellular injury, such as that caused by exposure to cadmium. The goal of this study was to define the role 6-O-sulfate plays in cellular responses to cadmium exposure in two pulmonary epithelial cancer cell lines (H292 and A549) and in normal human primary alveolar type II (hAT2) cells. Sulfate levels were modified by transduced transient over-expression of 6-O-endosulfatase (HSulf-1), a membrane-bound enzyme which specifically removes 6-O-sulfate groups from HSPG side chains. Results showed that cadmium decreased cell viability and activated apoptosis pathways at low concentrations in hAT2 cells but not in the cancer cells. HSulf-1 over-expression, on the contrary, decreased cell viability and activated apoptosis pathways in H292 and A549 cells but not in hAT2 cells. When combined with cadmium, HSulf-1 over-expression further decreased cell viability and exacerbated the activation of apoptosis pathways in the transformed cells but did not add to the toxicity in hAT2 cells. The finding that HSulf-1 sensitizes these cancer cells and intensifies the injury induced by cadmium suggests that 6-O-sulfate groups on HSPGs may play important roles in protection against certain environmental toxicants, such as heavy metals.}, number={1}, journal={TOXICOLOGY AND APPLIED PHARMACOLOGY}, author={Zhang, Huiying and Newman, Donna R. and Bonner, James C. and Sannes, Philip L.}, year={2012}, month={Nov}, pages={27–42} }
 @article{meuten_hickey_franklin_grossi_tobias_newman_jennings_correa_sannes_2012, title={WNT7B in fibroblastic foci of idiopathic pulmonary fibrosis}, volume={13}, ISSN={1465-9921}, url={http://dx.doi.org/10.1186/1465-9921-13-62}, DOI={10.1186/1465-9921-13-62}, abstractNote={Abstract}, number={1}, journal={Respiratory Research}, publisher={Springer Nature}, author={Meuten, Travis and Hickey, Ariel and Franklin, Katherine and Grossi, Brian and Tobias, Jeremy and Newman, Donna R and Jennings, Samuel H and Correa, Maria and Sannes, Philip L}, year={2012}, pages={62} }
 @article{dush_mciver_parr_young_fisher_newman_sannes_hauck_deiters_nascone-yoder_2011, title={Heterotaxin: A TGF-beta Signaling Inhibitor Identified in a Multi-Phenotype Profiling Screen in Xenopus Embryos}, volume={18}, ISSN={["1879-1301"]}, DOI={10.1016/j.chembiol.2010.12.008}, abstractNote={Disruptions of anatomical left-right asymmetry result in life-threatening heterotaxic birth defects in vital organs. We performed a small molecule screen for left-right asymmetry phenotypes in Xenopus embryos and discovered a pyridine analog, heterotaxin, which disrupts both cardiovascular and digestive organ laterality and inhibits TGF-β-dependent left-right asymmetric gene expression. Heterotaxin analogs also perturb vascular development, melanogenesis, cell migration, and adhesion, and indirectly inhibit the phosphorylation of an intracellular mediator of TGF-β signaling. This combined phenotypic profile identifies these compounds as a class of TGF-β signaling inhibitors. Notably, heterotaxin analogs also possess highly desirable antitumor properties, inhibiting epithelial-mesenchymal transition, angiogenesis, and tumor cell proliferation in mammalian systems. Our results suggest that assessing multiple organ, tissue, cellular, and molecular parameters in a whole organism context is a valuable strategy for identifying the mechanism of action of bioactive compounds.}, number={2}, journal={CHEMISTRY & BIOLOGY}, author={Dush, Michael K. and McIver, Andrew L. and Parr, Meredith A. and Young, Douglas D. and Fisher, Julie and Newman, Donna R. and Sannes, Philip L. and Hauck, Marlene L. and Deiters, Alexander and Nascone-Yoder, Nanette}, year={2011}, month={Feb}, pages={252–263} }
 @article{apparao_newman_zhang_khosla_randell_sannes_2010, title={Temporal Changes in Expression of FoxA1 and Wnt7A in Isolated Adult Human Alveolar Epithelial Cells Enhanced by Heparin}, volume={293}, ISSN={["1932-8494"]}, DOI={10.1002/ar.20805}, abstractNote={Abstract}, number={6}, journal={ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY}, author={Apparao, K. B. C. and Newman, Donna R. and Zhang, Huiying and Khosla, Jody and Randell, Scott H. and Sannes, Philip L.}, year={2010}, month={Jun}, pages={938–946} }
 @article{gabr_reed_newman_pohl_khosla_sannes_2007, title={Alterations in cytoskeletal and immune function-related proteome profiles in whole rat lung following intratracheal instillation of heparin}, volume={8}, ISSN={["1465-993X"]}, DOI={10.1186/1465-9921-8-36}, abstractNote={Abstract}, journal={RESPIRATORY RESEARCH}, author={Gabr, Amir A. and Reed, Mathew and Newman, Donna R. and Pohl, Jan and Khosla, Jody and Sannes, Philip L.}, year={2007}, month={May} }
 @article{newman_walsh_apparao_sannes_2007, title={Fibroblast growth factor-binding protein and N-deacetylase/N-sulfotransferase-1 expression in type II cells is modulated by heparin and extracellular matrix}, volume={293}, ISSN={["1522-1504"]}, DOI={10.1152/ajplung.00211.2007}, abstractNote={ Fibroblast growth factors (FGFs) play critical roles in development, maintenance, and repair following injury or disease in the lung. Their activity is modulated by a variety of factors, including FGF-binding protein (FGF-BP; HBp-17) and N-deacetylase/ N-sulfotransferase-1 (NDST-1). Functionally, FGF-BP shuttles FGFs from binding sites in ECMs to cell surfaces and enhances FGF binding and signaling, whereas NDST-1 adds sulfate groups to FGF coreceptor proteoglycans and modulates alveolar type II (ATII) cell maturation and differentiation. Since the sulfated nature of ECMs is a critical determinant of their relationship with FGFs, we predicted that ECMs and their sulfation would modulate the expression of FGF-BP and NDST-1. To examine this question, selected culture conditions of rat ATII cells were manipulated [with and without coculture with rat lung fibroblasts (RLFs)] by treatment with heparin or sodium chlorate (inhibitor of sulfation) for 24–96 h. In addition, ECMs biosynthesized by RLFs for up to 10 days before coculture were used as model intervening barriers to communication between alveolar cells and fibroblasts. FGF-BP expression was enhanced in ATII cells by coculture with RLF cells and least suppressed by desulfated heparin. NDST-1 expression in ATII cells was most sensitive to the amount of sulfation in medium and ECM and enhanced by fully sulfated heparin. Preformed ECM appears to supply factors that modify subsequent treatment effects. These results demonstrate a potentially important modulatory influence of sulfated ECMs and fibroblasts on FGF-BP and NDST-1 at the gene expression level. }, number={5}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Newman, Donna R. and Walsh, Eric and Apparao, K. B. C. and Sannes, Philip L.}, year={2007}, month={Nov}, pages={L1314–L1320} }
 @article{leiner_newman_li_walsh_khosla_sannes_2006, title={Heparin and fibroblast growth factors affect surfactant protein gene expression in type II cells}, volume={35}, DOI={10.1165/rcmb.2006-01590C}, number={5}, journal={American Journal of Respiratory Cell and Molecular Biology}, author={Leiner, K. A. and Newman, D. and Li, C. M. and Walsh, E. and Khosla, J. and Sannes, P. L.}, year={2006}, pages={611–618} }
 @article{newman_li_simmons_khosla_sannes_2004, title={Heparin affects signaling pathways stimulated by fibroblast growth factor-1 and-2 in type II cells}, volume={287}, ISSN={["1522-1504"]}, DOI={10.1152/ajplung.00284.2003}, abstractNote={Undersulfation of the basement membrane matrix of alveolar type II (AT2) cells compared with that of neighboring type I cells is believed to account for some of the known morphological and functional differences between these pneumocytes. Heparin, a model for sulfated components of basement membrane matrices, is known to inhibit fibroblast growth factor (FGF)-2-stimulated DNA synthesis as well as gene expression of FGF-2 and its receptor in AT2 cells. To determine whether these end points result from specific effects of heparin on FGF-related signaling pathways, isolated rat AT2 cells were treated with 100 ng/ml FGF-1 or FGF-2 in the presence of up to 500 μg/ml heparin. In addition, experiments were done on cells grown in the presence of 20 mM sodium chlorate (sulfation inhibitor). High-dose heparin reduced FGF-1- or FGF-2-stimulated phosphorylation of mitogen-activated protein kinase kinases (MEK1/2), p44/42 mitogen-activated protein kinases (MAPK/ERK1/2), stress-activated protein kinase/c-Jun NH2-terminal kinase, Akt/protein kinase B, and p90RSK. FGF-2-stimulated signaling was more sensitive to heparin's effects than was signaling stimulated by FGF-1. Heparin had an additive effect on the reduced [3H]thymidine incorporation in FGF-2-treated AT2 cells caused by inhibition of the MEK/ERK pathway by the MEK inhibitor PD-98059. The data suggest that heparin's known capacity to alter DNA synthesis and, possibly, other biological end points is realized via cross talk between multiple signaling pathways.}, number={1}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Newman, DR and Li, CM and Simmons, R and Khosla, J and Sannes, PL}, year={2004}, month={Jul}, pages={L191–L200} }
 @article{evans_fanucchi_baker_van winkle_pantle_nishio_schelegle_gershwin_miller_hyde_et al._2003, title={Atypical development of the tracheal basement membrane zone of infant rhesus monkeys exposed to ozone and allergen}, volume={285}, ISSN={["1040-0605"]}, DOI={10.1152/ajplung.00175.2003}, abstractNote={ Development of the basement membrane zone (BMZ) occurs postnatally in the rhesus monkey. The purpose of this study was to determine whether house dust mite allergen (HDMA) plus ozone altered this process. Rhesus monkeys were exposed to a regimen of HDMA and/or ozone or filtered air for 6 mo. To detect structural changes in the BMZ, we measured immunoreactivity of collagen I. To detect functional changes in the BMZ, we measured perlecan and fibroblast growth factor-2 (FGF-2). We also measured components of the FGF-2 ternary signaling complex [fibroblast growth factor receptor-1 (FGFR-1) and syndecan-4]. The width of the BMZ was irregular in the ozone groups, suggesting atypical development of the BMZ. Perlecan was also absent from the BMZ. In the absence of perlecan, FGF-2 was not bound to the BMZ. However, FGF-2 immunoreactivity was present in basal cells, the lateral intercellular space (LIS), and attenuated fibroblasts. FGFR-1 immunoreactivity was downregulated, and syndecan-4 immunoreactivity was upregulated in the basal cells. This suggests that FGF-2 in basal cells and LIS may be bound to the syndecan-4. We conclude that ozone and HDMA plus ozone effected incorporation of perlecan into the BMZ, resulting in atypical development of the BMZ. These changes are associated with specific alterations in the regulation of FGF-2, FGFR-1, and syndecan-4 in the airway epithelial-mesenchymal trophic unit, which may be associated with the developmental problems of lungs associated with exposure to ozone. }, number={4}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Evans, MJ and Fanucchi, MV and Baker, GL and Van Winkle, LS and Pantle, LM and Nishio, SJ and Schelegle, ES and Gershwin, LJ and Miller, LA and Hyde, DM and et al.}, year={2003}, month={Oct}, pages={L931–L939} }
 @article{li_newman_cesta_tompkins_khosla_sannes_2003, title={Modulation of fibroblast growth factor expression and signal transduction in type II cells}, volume={123}, ISSN={["0012-3692"]}, DOI={10.1378/chest.123.3_suppl.429S}, abstractNote={repair and wound healing. PDGFs are synthesized and secreted by most inflammatory cell types present within the milieu of the asthmatic airway. We have previously reported that airway fibroblasts from severe asthmatics produce more type I procollagen in response to PDGF stimulation as compared to patients with mild asthma and normal control subjects; therefore, we hypothesized that the enhanced responsiveness to PDGFs in patients with severe asthma is linked to an increased expression of PDGF receptors. In an ongoing study, 5 subjects with severe asthma, 10 subjects with mild-to-moderate asthma, and 6 normal control subjects underwent bronchoscopy with endobronchial biopsy. Biopsies were placed in Dulbecco’s modified Eagle’s serum supplemented with fetal bovine serum (10%), streptomycin (100 g/mL), penicillin (10,000 U/mL), and gentamicin (100 g/mL), and cultured until fibroblast growth was established at 50% confluency (approximately 8 to 20 days). Immunostaining with vimentin (Dako; Carpenteria, CA), Ab-1 (Calbiochem; San Diego, CA) and -smooth muscle actin (Dako) confirmed fibroblast identity. To determine baseline fibroblast expression of PDGF receptors (PDGFRs) [PDGFRand PDGFR], we developed a sandwich enzyme-linked immunosorbent assay for these receptors that quantifies receptor protein levels in fibroblast cell lysates. Receptor protein levels were expressed in nanograms per 100 g of total cell protein. There were no significant differences in baseline expression of PDGFRbetween the groups (severe, 7.6 ng/100 g protein; mild to moderate, 12.50 ng/100 g protein; normal control, 11.33 ng/100 g protein; p 0.35). However, there was a significantly greater baseline expression of PDGFRin the severe asthmatic group, as compared to both the mild/moderate asthmatic and normal control groups (severe, 15.20 ng/100 g protein; mild-to-moderate, 13.30 ng/100 g protein; normal control, 3.67 ng/100 g protein; p 0.0024). Our data suggests that airway fibroblasts from severe asthmatics may be of a synthetic phenotype, with altered capabilities in collagen production, as compared to those from patients with mild-to-moderate asthma and normal control subjects, and this may be driven by an increased expression of PDGFR. Modulation of Fibroblast Growth Factor Expression and Signal Transduction in Type II Cells*}, number={3}, journal={CHEST}, author={Li, CM and Newman, D and Cesta, M and Tompkins, L and Khosla, J and Sannes, PL}, year={2003}, month={Mar}, pages={429S–429S} }
 @article{pagan_khosla_li_sannes_2002, title={Effect of growth factor-fibronectin matrix interaction on rat type II cell adhesion and DNA synthesis}, volume={28}, ISSN={["0190-2148"]}, DOI={10.1080/019021402753462013}, abstractNote={Type II cells attach, migrate, and proliferate on a provisional fibronectin-rich matrix during alveolar wall repair after lung injury. The combination of cell-substratum interactions via integrin receptors and exposure to local growth factors are likely to initiate the signals required for cell proliferation, differentiation, reepithelialization, and ultimate restoration of the alveolar wall structure. Accordingly, primary cultured type II cells have been shown to bind fibronectin, in part through the α 5 β 1 integrin, and to respond to growth factors that induce type II cell proliferation, such as fibroblast growth factor 1 (FGF-1). The purpose of this study was to determine whether or not FGF-1 modifies type II cell attachment to fibronectin, and if together they affect DNA synthesis. Attachment assays showed that FGF-1 treatment enhanced type II cell adhesion to fibronectin. This effect correlated with an increase in β 1 integrin cell surface expression, and with the formation of cytoskeletal stabilizing structures such as lamellipodial extensions and stress fibers. FGF-1 also induced an increase in thymidine in corporation into DNA. Together FGF-1 and fibronectin appear to promote adhesion, cytoskeletal organization, and in creased DNA synthesis, and in this way influence cell-substratum interactions and signaling during alveolar repair.}, number={2}, journal={EXPERIMENTAL LUNG RESEARCH}, author={Pagan, I and Khosla, J and Li, CM and Sannes, PL}, year={2002}, month={Mar}, pages={69–84} }
 @article{evans_fanucchi_van winkle_baker_murphy_nishio_sannes_plopper_2002, title={Fibroblast growth factor-2 during postnatal development of the tracheal basement membrane zone}, volume={283}, ISSN={["1040-0605"]}, DOI={10.1152/ajplung.00180.2002}, abstractNote={ Thickening of the basement membrane zone (BMZ) is a characteristic of several airway diseases; however, very little is known about how this process occurs. The purpose of this study was to define development of the BMZ in the trachea of growing rhesus monkeys at 1, 2, 3, and 6 mo of age. We measured immunoreactivity of collagen types I, III, and V to detect structural changes in the developing BMZ. To detect more dynamic, functional components of the epithelial-mesenchymal trophic unit, we evaluated the distribution of perlecan, fibroblast growth factor-2 (FGF-2), and fibroblast growth factor receptor-1 (FGFR-1). One-month-old monkeys had a mean collagen BMZ width of 1.5 ± 0.7 μm that increased to 4.4 ± 0.4 μm in 6-mo-old monkeys. Perlecan was localized in the BMZ of the epithelium at all ages. FGF-2 was strongly expressed in basal cells at 1–3 mo. At 6 mo, FGF-2 was expressed throughout the BMZ and weakly in basal cells. FGFR-1 immunoreactivity was expressed by basal cells and cilia and weakly in the nuclei of columnar cells at all time points. These data indicate that development of the BMZ is a postnatal event in the rhesus monkey that involves FGF-2. }, number={6}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Evans, MJ and Fanucchi, MV and Van Winkle, LS and Baker, GL and Murphy, AE and Nishio, SJ and Sannes, PL and Plopper, CG}, year={2002}, month={Dec}, pages={L1263–L1270} }
 @article{li_newman_khosla_sannes_2002, title={Heparin inhibits DNA synthesis and gene expression in alveolar type II cells}, volume={27}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2002-0002OC}, abstractNote={Responses of isolated type II alveolar cells to fibroblast growth factors (FGF) have been shown to be sensitive to the level of sulfation in extracellular matrix (ECM) substrata. These observations may reflect the specific in situ distribution and level of sulfation of ECM within the alveolar basement membranes (ABM) associated with type II cells. The goal of this study was to determine if the model sulfated ECM heparin modified DNA synthesis and gene expression by type II cells in a concentration dependent-manner. Isolated rat type II cells were exposed to different concentrations of heparin (0.005-500 micro g/ml) in serum-free medium for 1-3 d with or without FGF-1 or FGF-2. The effects of heparin were examined by [(3)H]thymidine incorporation into DNA, total cell protein, cell number, and selected gene expression. Results indicated that heparin inhibited [(3)H]thymidine uptake in a concentration-dependent manner. Total protein, cell number, and FGF-2 protein expression and mRNA of FGF-1, -2, and FGF receptor-2 detected by reverse transcriptase-polymerase chain reaction were decreased by heparin. These results demonstrate that sulfated molecules in the ABM may play important regulatory role(s) in selected type II cell activities during normal cell homeostasis, turnover, and repair after lung injury.}, number={3}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Li, CM and Newman, D and Khosla, J and Sannes, PL}, year={2002}, month={Sep}, pages={345–352} }
 @article{wang_sakamoto_khosla_sannes_2002, title={Pre- and postnatal lung development, maturation, and plasticity: Detection of chondroitin sulfates and decorin in developing fetal and neonatal rat lung}, volume={282}, ISSN={["1522-1504"]}, DOI={10.1152/ajplung.00160.2001}, abstractNote={Chondroitin sulfates and their related proteoglycans are components of extracellular matrix that act as key determinants of growth and differentiation characteristics of developing lungs. Changes in their immunohistochemical distribution during progressive organ maturation were examined with monospecific antibodies to chondroitin sulfate, a nonbasement membrane chondroitin sulfate proteoglycan, and the specific chondroitin sulfate-containing proteoglycan decorin in whole fetuses and lungs from newborn and adult rats. Alveolar and airway extracellular matrix immunostained heavily in the prenatal rat for both chondroitin sulfate and chondroitin sulfate proteoglycan, whereas decorin was confined to developing airways and vessels. These sites retained their respective levels of reactivity with all antibodies through 1–10 days postnatal but thereafter became progressively more diminished and focal in alveolar regions. The heavy staining seen early in development was interpreted to reflect a significant and wide distribution of chondroitin sulfates, chondroitin sulfate proteoglycans, and decorin in rapidly growing tissues, whereas the reduced and more focal reactivity observed at later time points coincided with known focal patterns of localization of fibrillar elements of the extracellular matrix and a more differentiated state.}, number={3}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Wang, YQ and Sakamoto, K and Khosla, J and Sannes, PL}, year={2002}, month={Mar}, pages={L484–L490} }
 @article{li_khosla_hoyle_sannes_2001, title={Transforming growth factor-beta(1) modifies fibroblast growth factor-2 production in type II cells}, volume={120}, ISSN={["0012-3692"]}, DOI={10.1378/chest.120.1_suppl.S60}, abstractNote={Transforming growth factor (TGF)-β 1 is an inflammatory cytokine that plays multiple roles in pulmonary fibrosis. In vascular epithelium, it has been shown to regulate production and activity of fibroblast growth factor (FGF)-2, a potent type II cell mitogen in the lung. Such a relationship could have important consequences in prefibrotic change in the lung alveolus, where reepithelialization of alveolar surfaces is crucial. The goal of this study was to determine if FGF-2 production by alveolar type II cells is modulated by TGF-β 1 or FGF-1, another type II cell mitogen. Isolated rat type II cells were exposed to 0 to 40 ng/mL of TGF-β 1 or 0 to 500 ng/mL of FGF-1 in serum-free medium for 1 to 3 days. Using a specific immunoassay, significant increases in FGF-2 protein in type II cell lysates were achieved after 1 day of exposure to 100 ng/mL of FGF-1 and after 3 days of treatment with 8 ng/mL of TGF-β 1 . Similarly, transcripts for FGF-2 were dramatically increased with TGF-β 1 or FGF-1, as were those for FGF receptor (FGFR)-1. These interactions were dramatically effected by the addition of heparin, a model sulfated extracellular matrix (ECM). Heparin as low as 0.01 mg/mL significantly downregulated expression of TGF-β 1 and FGF-1–stimulated FGF-2 and FGFR-1. These results demonstrate important regulatory links between FGF-2, sulfated ECMs, and both TGF-β 1 and FGF-1, which could contribute to the modulation of normal cell turnover, development, and repair processes attendant to fibrosis in the lung.}, number={1}, journal={CHEST}, author={Li, CM and Khosla, J and Hoyle, P and Sannes, PL}, year={2001}, month={Jul}, pages={60S–61S} }
 @article{zhang_rice_adler_sannes_martin_gladwell_koo_gray_bonner_2001, title={Vanadium stimulates human bronchial epithelial cells to produce heparin-binding epidermal growth factor-like growth factor - A mitogen for lung fibroblasts}, volume={24}, ISSN={["1044-1549"]}, DOI={10.1165/ajrcmb.24.2.4096}, abstractNote={The bronchial epithelium is a potential source of growth factors that could mediate airway fibrosis during the progression of diseases such as asthma and chronic bronchitis. We report that conditioned medium (CM) from normal human bronchial epithelial cells (NHBECs) contains mitogenic activity for human lung fibroblasts that is blocked by the epidermal growth factor receptor (EGF-R) tyrosine kinase inhibitor AG1478 and by neutralizing antibodies raised against heparin-binding epidermal growth factor-like growth factor (HB-EGF). Neutralizing antibodies against other EGF-R ligands (EGF and transforming growth factor-alpha) or other antibodies against growth factors (platelet-derived growth factors, insulin-like growth factor-1) had no affect on the mitogenic activity of NHBEC-CM. HB-EGF messenger RNA (mRNA) expression in NHBEC was detected by reverse transcriptase/polymerase chain reaction and Northern blot analysis. HB-EGF protein was detected by enzyme-linked immunosorbent assay. Vanadium pentoxide (V2O5), a fibrogenic metal associated with occupational asthma, caused a several-fold increase in HB-EGF mRNA expression and protein, whereas the inert metal titanium dioxide had no effect on HB-EGF expression. V2O5-induced HB-EGF mRNA expression was inhibited by the EGF-R tyrosine kinase inhibitor AG1478, the p38 mitogen-activated protein (MAP) kinase inhibitor SB203580, and the MAP kinase kinase inhibitor PD98059. Finally, HB-EGF induced the production of fibroblast growth factor (FGF)-2 by human lung fibroblasts and anti-FGF-2 antibody partially blocked the mitogenic activity of NHBEC-CM on fibroblasts. These data suggest that HB-EGF is a fibroblast mitogen produced by NHBECs and that induction of an FGF-2 autocrine loop in fibroblasts by HB-EGF accounts for part of this mitogenic activity.}, number={2}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Zhang, LM and Rice, AB and Adler, K and Sannes, P and Martin, L and Gladwell, W and Koo, JS and Gray, TE and Bonner, JC}, year={2001}, month={Feb}, pages={123–131} }
 @article{bonner_zhang_sannes_martin_gladwell_koo_gray_adler_2000, title={Induction of heparin-binding epidermal growth factor (HB-EGF) mRNA in normal human bronchial epithelial cells by metal-induced oxidative stress.}, volume={161}, journal={American Journal of Respiratory and Critical Care Medicine}, author={Bonner, J. C. and Zhang, L. and Sannes, P. and Martin, L. and Gladwell, W. and Koo, J.-S. and Gray, T. and Adler, K.}, year={2000}, pages={A149} }
 @article{li_khosla_pagan_hoyle_sannes_2000, title={TGF-beta 1 and fibroblast growth factor-1 modify fibroblast growth factor-2 production in type II cells}, volume={279}, ISSN={["1040-0605"]}, DOI={10.1152/ajplung.2000.279.6.l1038}, abstractNote={ Fibroblast growth factor (FGF)-2, which stimulates DNA synthesis by type II cells in the lung, has been shown to be regulated by transforming growth factor (TGF)-β1, an important inflammatory cytokine, in vascular epithelium. The goal of this study was to determine if FGF-2 production by alveolar type II cells is modulated by TGF-β1 or FGF-1, which also stimulates DNA synthesis by type II cells. Isolated rat type II cells were exposed to 0–40 ng/ml of TGF-β1 or 0–500 ng/ml of FGF-1 in serum-free medium for 1–5 days. With a specific immunoassay, significant increases of FGF-2 protein in type II cell lysates to levels above those in control cells were achieved after 1 day of exposure to 100 ng/ml of FGF-1 and after 3 days of treatment with 8 ng/ml of TGF-β1. Similarly, transcripts for FGF-2 were dramatically increased above those in control cells with TGF-β1 or FGF-1, as were those for FGF receptor-1. These results demonstrate important regulatory links between FGF-2 and both TGF-β1 and FGF-1 in the alveolar epithelium that could contribute to the regulation of normal cell turnover, development, and the repair processes after injury in the lung. }, number={6}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Li, CM and Khosla, J and Pagan, I and Hoyle, P and Sannes, PL}, year={2000}, month={Dec}, pages={L1038–L1046} }
 @article{evans_van winkle_fanucchi_toskala_luck_sannes_plopper_2000, title={Three-dimensional organization of the lamina reticularis in the rat tracheal basement membrane zone}, volume={22}, ISSN={["1535-4989"]}, DOI={10.1165/ajrcmb.22.4.3913}, abstractNote={The airway basement membrane zone is a region specialized for the attachment of the epithelium with the matrix. The epithelium is attached to the lamina densa, which, in turn, is connected to types I and III collagen of the lamina reticularis with anchoring fibrils. The purpose of this study was to define the three-dimensional organization of the structural proteins of the lamina reticularis in the rat trachea. We approached this problem by using whole mounts to look down on the flat surface of the basement-membrane zone rather than a cross section of its thin profile. Fluorescent microscopy with long working distance water immersion objectives and scanning electron microscopy revealed that the structural proteins are arranged as a mat of large fibers oriented along the longitudinal axis of the airway. Smaller fibers are crosslinked with the larger fibers to complete this structure. Other small fibers are oriented around the large fibers and an amorphous material covers individual fibers. The large fibers oriented along the longitudinal axis of the airway are consistent with prior descriptions of fibers composed of collagen III with some collagen I and V; small fibers encircling the large fibers may be collagen VI. The crosslinking fibers are made up of elastin and probably elastin-associated microfibrils. The amorphous proteins covering the fibrous framework may contain proteoglycans and other nonstructural proteins reported to be in the lamina reticularis. The present studies demonstrate that the structural proteins of the lamina reticularis in the rat trachea are arranged as fibers in a highly organized manner.}, number={4}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Evans, MJ and Van Winkle, LS and Fanucchi, MV and Toskala, E and Luck, EC and Sannes, PL and Plopper, CG}, year={2000}, month={Apr}, pages={393–397} }
 @article{zhang_adler_sannes_bonner_1999, title={Normal human bronchial epithelial cells produce heparin-binding epidermal growth factor (HB-EGF), a mitogen for human lung fibroblasts in vitro.}, volume={159}, journal={American Journal of Respiratory and Critical Care Medicine}, author={Zhang, L. and Adler, K. B. and Sannes, P. and Bonner, J. C.}, year={1999}, pages={A508} }
 @article{sannes_khosla_li_pagan_1998, title={Sulfation of extracellular matrices modifies growth factor effects on type II cells on laminin substrata}, volume={275}, ISSN={["1040-0605"]}, DOI={10.1152/ajplung.1998.275.4.l701}, abstractNote={The alveolar basement membrane contains a variety of extracellular matrix (ECM) molecules, including laminin and sulfated glycosaminoglycans of proteoglycans. These mixtures exist within microdomains of differing levels of sulfate, which may specifically interact to be key determinants of the known capacity of the type II cell to respond to certain growth factors. Isolated type II cells were exposed to either acidic fibroblast growth factor (FGF-1), basic fibroblast growth factor (FGF-2), or keratinocyte growth factor (KGF; FGF-7) on culture wells precoated with laminin alone or in combination with chondroitin sulfate (CS), high-molecular-weight heparin, or their desulfated forms. Desulfated heparin significantly elevated FGF-1- and FGF-2-stimulated DNA synthesis, whereas desulfated CS and N-desulfated heparin elevated FGF-7-stimulated DNA synthesis by type II cells on laminin substrata. When FGF-1 was mixed into the various test matrix substrata, DNA synthesis was significantly increased in all cases. These results demonstrated that decreased levels of sulfate in ECM substrata act to upregulate responses to heparin-binding growth factors by alveolar epithelial cells on laminin substrata.}, number={4}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Sannes, PL and Khosla, J and Li, CM and Pagan, I}, year={1998}, month={Oct}, pages={L701–L708} }
 @article{sannes_wang_1997, title={Basement membranes and pulmonary development}, volume={23}, ISSN={["0190-2148"]}, DOI={10.3109/01902149709074023}, abstractNote={Basement membranes (BM) are specialized extracellular matrices (ECM) which serve as complex interfaces between epithelia, peripheral nerves, or muscle cells and their surrounding tissue microenvironments. Their composition is known to include type IV collagen, laminin, entactin, heparan sulfate proteoglycan (HSPG, perlecan), and chondroitin sulfate proteoglycan (CSPG). By immunohistochemistry, collagen IV, laminin, and entactin are detectable from day 14 of gestation on, and become progressively more prominent with time. Perleaan has not been examined in prentatal lungs, but is widely distributed and abundant in all lung MBs from birth throughout development. CSPG has a somewhat discontinuous and lightly reactive appearance in alveolar BMs at birth but the staining becomes continuous and darker in the adult. This contrasts with glycosaminoglycan, chondroitin sulfate, which is prominently expressed in prenatal and early postnatal stages, but progressively diminishes with advancing development. As an interface between cell populations and surrounding ECMs, BMs act as a physical barrier to some cells and molecules, while serving as attachment points and binding sites for others. Basic fibroblast growth factor is an example of the latter, because it localizes with all BM components by immunostaining throughout development and reflects the multifactorial array of potential effectors in the complex processes of proliferation and differentiation.}, number={2}, journal={EXPERIMENTAL LUNG RESEARCH}, author={Sannes, PL and Wang, J}, year={1997}, pages={101–108} }
 @article{sannes_khosla_peters_1997, title={Biosynthesis of sulfated extracellular matrices by alveolar type II cells increases with time in culture}, volume={273}, ISSN={["1040-0605"]}, DOI={10.1152/ajplung.1997.273.4.l840}, abstractNote={The aim of this study was to determine the extent to which sulfate incorporated into biosynthesized basement membrane (BM) components increased as isolated type II cells progress toward a more type I cell-like phenotype from 7 to 21 days in culture. Specific sulfate cytochemistry, using high iron diamine, showed that type I-like cells in 21-day cultures deposited a more highly sulfated extracellular matrix. Biosynthetic labeling experiments using [35S]cysteine or [35S]sulfate as precursors confirmed the increased capacity of 21-day type I-like cells to biosynthesize sulfated BM components compared with type II-like cells in 7-day cultures, including a novel sulfated laminin. These biochemical changes in sulfation of BM components coincide with the established phenotypic transition from type II to type I cells during prolonged culture. More importantly, the data suggest that regulation of sulfation constitutes a potential mechanism by which type I and type II cells alter their environment in such a manner as to stabilize phenotype and modulate responses to growth factors.}, number={4}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Sannes, PL and Khosla, J and Peters, BP}, year={1997}, month={Oct}, pages={L840–L847} }
 @article{adler_menard_sannes_1996, title={Airway epithelium: A primary source for growth factors related to development of fibrosis?}, volume={9}, journal={Proceedings of the 9th International Colloquium on Lung Fibrosis}, author={Adler, K. B. and Menard, M. and Sannes, P. L.}, year={1996}, pages={29} }
 @article{sannes_peters_adler_1991, title={Specific interactions with extracellular matrix may influence epithelial repair mechanisms in the pulmonary alveolus.}, volume={99}, journal={Chest}, author={Sannes, P. and Peters, B. and Adler, K.}, year={1991}, pages={70S–71} }
 @article{adler_peters_krunkosky_sannes_1990, title={Interactions between extracellular matrix, airway and alveolar epithelium: alterations in fibrosis and possible pathogenetic significance.}, volume={6}, journal={Proceedings of the Sixth International Colloquium Pulmonary Fibrosis.}, author={Adler, K. B. and Peters, B. P. and Krunkosky, T. and Sannes, P. L.}, year={1990}, pages={39} }
 @article{sannes_peters_adler_1990, title={Specific interactions with extracellular matrix may influence epithelial repair mechanisms in the pulmonary alveolus.}, volume={30}, journal={Proceedings of the 30th Aspen Lung Conference.}, author={Sannes, P. and Peters, B. and Adler, K.}, year={1990}, pages={24} }