@article{miller_lankford_adler_brody_2010, title={Mesenchymal Stem Cells Require MARCKS Protein for Directed ChemotaxisIn Vitro}, volume={43}, ISSN={1044-1549 1535-4989}, url={http://dx.doi.org/10.1165/rcmb.2010-0015RC}, DOI={10.1165/rcmb.2010-0015rc}, abstractNote={Mesenchymal stem cells (MSCs) reside within tissues such as bone marrow, cord blood, and dental pulp and can differentiate into other mesenchymal cell types. Differentiated MSCs, called circulating fibrocytes, have been demonstrated in human lungs and migrate to injured lung tissue in experimental models. It is likely that MSCs migrate from the bone marrow to sites of injury by following increasing chemokine concentrations. In the present study, we show that primary mouse bone marrow mesenchymal stem cells (BM-MSCs) exhibit directed chemotaxis through transwell inserts toward increasing concentrations of the chemokines complement component 5a, stromal cell-derived factor-1alpha, and monocyte chemotactic protein-1. Prior research has indicated that myristoylated alanine-rich C kinase substrate (MARCKS) protein is critically important for motility in macrophages, neutrophils, and fibroblasts, and here we investigated a possible role for MARCKS in BM-MSC directed chemotaxis. The presence of MARCKS in these cells as well as in human cord blood MSC was verified by Western blotting, and MARCKS was rapidly phosphorylated in these cells after exposure to chemokines. A synthetic peptide that inhibits MARCKS function attenuated, in a concentration-dependent manner, directed chemotaxis of BM-MSCs, while a missense control peptide had no effect. Our results illustrate, for the first time, that MARCKS protein plays an integral role in BM-MSC-directed chemotaxis in vitro.}, number={3}, journal={American Journal of Respiratory Cell and Molecular Biology}, publisher={American Thoracic Society}, author={Miller, Jeffrey D. and Lankford, Susan M. and Adler, Kenneth B. and Brody, Arnold R.}, year={2010}, month={Sep}, pages={253–258} }
 @article{salazar_lankford_brody_2009, title={Mesenchymal stem cells produce Wnt isoforms and TGF-beta(1) that mediate proliferation and procollagen expression by lung fibroblasts}, volume={297}, ISSN={["1522-1504"]}, DOI={10.1152/ajplung.90347.2008}, abstractNote={ Studies have been carried out previously to determine whether mesenchymal stem cells (MSC) influence the progression of pulmonary fibrosis. Here, we asked whether MSC (derived from mouse bone marrow and human umbilical cord blood) produce factors that mediate lung fibroblast (LF) growth and matrix production. MSC-conditioned media (CM) were found by ELISA to contain significant amounts of PDGF-AA and transforming growth factor-β1 (TGF-β1). Proliferation was increased in a concentration-dependent manner in LF cell lines and primary cells cultured in MSC-CM, but neither anti-PDGF antibodies nor PDGF receptor-specific antibodies affected proliferation, nor did a number of other antibodies to well-known mitogenic factors. However, proliferation was significantly inhibited by the Wnt signaling antagonist, secreted frizzled related protein-1 (sFRP-1). In addition, anti-Wnt1 and anti-Wnt2 antibodies attenuated MSC-CM-induced proliferation, and increased expression of Wnt7b was identified. As would be expected in cells activated by Wnt, nuclear β-catenin was increased. The amount of TGF-β1 in MSC-CM and its biological activity were revealed by activation at acidic pH. The stem cells synthesized and released TGF-β1 that increased α1-procollagen gene expression by LF target cells. Addition of anti-TGF-β to the MSC-CM blocked upregulation of collagen gene expression. These data demonstrate that MSC from mice and humans produce Wnt proteins and TGF-β1 that respectively stimulate LF proliferation and matrix production, two hallmarks of fibroproliferative lung disease. It will be essential to determine whether these factors can play a role in attempts to use MSC for therapeutic approaches. }, number={5}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Salazar, Keith D. and Lankford, Susan M. and Brody, Arnold R.}, year={2009}, month={Nov}, pages={L1002–L1011} }
 @article{lankford_petty_la voy_reckling_tompkins_dean_2008, title={Cloning of feline FOXP3 and detection of expression in CD4+CD25+ regulatory T cells}, volume={122}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2007.11.007}, abstractNote={Regulatory T cells (Treg) are increased and directly infected by feline immunodeficiency virus (FIV) and likely play a role in other feline autoimmune, neoplastic, and infectious diseases. Phenotypically, Treg are best characterized by surface expression of CD4 and CD25 and intranuclear expression of the forkhead transcription factor Foxp3. Our objective was to clone and sequence feline FOXP3 for the purpose of developing assays to enhance studies of feline Treg. We determined the feline FOXP3 is 1293 nucleotides in length and codes for a protein that shares high homology to other species. A splice variant devoid of exon 2 was also identified. A real-time PCR assay was developed and used to show Foxp3 mRNA expression occurs primarily in CD4+CD25+ T cells. Two cross-reacting antibodies were identified by immunocytochemical staining of HEK293 cells transfected with feline FOXP3. The antibody labeling confirmed the nuclear localization of the protein. A flow cytometric assay was also validated and used to correlate the phenotypic and functional characteristics of feline Treg induced by treatment of lymph node lymphocytes with flagellin or LPS in combination with mitogen or IL2. Together, these studies provide useful tools to further investigate Foxp3 and Tregs in cats.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Lankford, Susan and Petty, Christopher and La Voy, Alora and Reckling, Stacie and Tompkins, Wayne and Dean, Gregg A.}, year={2008}, month={Mar}, pages={159–166} }
 @article{smithberg_fogle_mexas_reckling_lankford_tompkins_dean_2008, title={In vivo depletion of CD4(+)CD25(+) regulatory T cells in cats}, volume={329}, ISSN={["0022-1759"]}, DOI={10.1016/j.jim.2007.09.015}, abstractNote={To establish a characterized model of regulatory T cell (Treg) depletion in the cat we assessed the kinetics of depletion and rebound in peripheral and central lymphoid compartments after treatment with anti-CD25 antibody as determined by cell surface markers and FOXP3 mRNA expression. An 82% decrease in circulating CD4+CD25+ Tregs was observed by day 11 after treatment. CD4+CD25+ cells were also reduced in the thymus (69%), secondary lymphoid tissues (66%), and gut (67%). Although CD4+CD25+ cells rebound by day 35 post-treatment, FOXP3 levels remain depressed suggesting anti-CD25 antibody treatment has a sustainable diminutive effect on the Treg population. To determine whether CD25+ Treg depletion strategies also deplete activated CD25+ effector cells, cats were immunized with feline immunodeficiency virus (FIV) p24-GST recombinant protein, allowing them to develop a measurable memory response, prior to depletion with anti-CD25 antibody. Anti-FIV p24-GST effector cell activity in peripheral blood after depletion was sustained as determined by antigen-specific T cell proliferation and humoral responses against FIV p24-GST with an ELISA for antigen-specific feline IgG. Furthermore, development of an anti-mouse response in Treg-depleted cats was similar to control levels indicating the retained capacity to respond to a novel antigen. We conclude that despite alterations in CD25+ cell levels during depletion, the feline immune system remains functional. We demonstrate here a model for the study of disease pathogenesis in the context of reduced numbers of immunosuppressive CD4+CD25+ Tregs throughout the feline immune system.}, number={1-2}, journal={JOURNAL OF IMMUNOLOGICAL METHODS}, author={Smithberg, S. Rochelle and Fogle, Jonathan E. and Mexas, Angela M. and Reckling, Stacie K. and Lankford, Susan M. and Tompkins, Mary B. and Dean, Gregg A.}, year={2008}, month={Jan}, pages={81–91} }
 @article{lankford_macchione_crews_mckane_akley_martin_2005, title={Modeling the airway epithelium in allergic asthma: Interleukin-13-induced effects in differentiated murine tracheal epithelial cells}, volume={41}, number={7}, journal={In Vitro Cellular & Developmental Biology. Animal}, author={Lankford, S. M. and Macchione, M. and Crews, A. L. and McKane, S. A. and Akley, N. J. and Martin, L. D.}, year={2005}, pages={217–224} }
 @article{lankford_bai_goldstein_2000, title={Cloning of canine cytochrome P450 2E1 CDNA: identification and characterization of two variant alleles}, volume={28}, number={8}, journal={Drug Metabolism and Disposition}, author={Lankford, S. M. and Bai, S. A. and Goldstein, J. A.}, year={2000}, pages={981–986} }
 @article{lankford_plummer_hellyer_christ_bai_1997, title={Pharmacokinetic-pharmacodynamic relations of losartan and EXP3174 in a porcine animal model}, volume={30}, ISSN={["1533-4023"]}, DOI={10.1097/00005344-199711000-00008}, abstractNote={The pharmacokinetics of losartan and EXP3174, an active metabolite of losartan, were evaluated in the anesthetized pig after both a single intravenous dose (3 mg/kg) and during constant intravenous infusion. The pharmacodynamic activities of losartan and EXP3174 were determined during constant intravenous infusion as the degree of inhibition of angiotensin II-induced increase in the diastolic pressure. The systemic plasma clearance of losartan was 22.1 +/- 4.4 ml/min/kg (mean +/- SEM) and had an apparent volume of distribution at steady state of 0.56 +/- 0.16 L/kg after a 3-mg/kg intravenous dose. The elimination half-life of losartan was 40 +/- 6 min. Less than 2% of the intravenous losartan doses was estimated to be present as unconjugated EXP3174. The plasma clearance of EXP3174 was approximately 50% that of losartan, 11.8 +/- 1.5 ml/min/kg, and had a smaller steady-state apparent volume of distribution, 0.18 +/- 0.04 L/kg. The elimination half-life for EXP3174 was slightly longer than that of losartan (52 min). The time course of the pharmacodynamic effects of losartan and EXP3174 closely followed their respective plasma concentrations. The apparent dissociation constant of EXP3174 to the angiotensin II receptor was estimated, based on the total plasma concentrations, to be approximately 5 times lower than that for losartan.}, number={5}, journal={JOURNAL OF CARDIOVASCULAR PHARMACOLOGY}, author={Lankford, SM and Plummer, D and Hellyer, P and Christ, DD and Bai, SA}, year={1997}, month={Nov}, pages={583–590} }