@article{wooten_lascelles_cook_law_blikslager_2010, title={Evaluation of the relationship between lesions in the gastroduodenal region and cyclooxygenase expression in clinically normal dogs}, volume={71}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.71.6.630}, DOI={10.2460/ajvr.71.6.630}, abstractNote={Abstract}, number={6}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Wooten, Jenna G. and Lascelles, B. Duncan X. and Cook, Vanessa L. and Law, J. Mac and Blikslager, Anthony T.}, year={2010}, month={Jun}, pages={630–635} }
 @article{wooten_blikslager_marks_law_graeber_lascelles_2009, title={Effect of nonsteroidal anti-inflammatory drugs with varied cyclooxygenase-2 selectivity on cyclooxygenase protein and prostanoid concentrations in pyloric and duodenal mucosa of dogs}, volume={70}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.70.10.1243}, DOI={10.2460/ajvr.70.10.1243}, abstractNote={Abstract}, number={10}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Wooten, Jenna G. and Blikslager, Anthony T. and Marks, Steve L. and Law, J. Mac and Graeber, Elizabeth C. and Lascelles, B. Duncan X.}, year={2009}, month={Oct}, pages={1243–1249} }
 @article{wooten_blikslager_ryan_marks_law_lascelles_2008, title={Cyclooxygenase expression and prostanoid production in pyloric and duodenal mucosae in dogs after administration of nonsteroidal anti-inflammatory drugs}, volume={69}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.69.4.457}, DOI={10.2460/ajvr.69.4.457}, abstractNote={Abstract}, number={4}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Wooten, Jenna G. and Blikslager, Anthony T. and Ryan, Kathleen A. and Marks, Steve L. and Law, J. Mac and Lascelles, B. Duncan X.}, year={2008}, month={Apr}, pages={457–464} }
 @article{moeser_klok_ryan_wooten_little_cook_blikslager_2007, title={Stress signaling pathways activated by weaning mediate intestinal dysfunction in the pig}, volume={292}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00197.2006}, DOI={10.1152/ajpgi.00197.2006}, abstractNote={Weaning in the piglet is a stressful event associated with gastrointestinal disorders and increased disease susceptibility. Although stress is thought to play a role in postweaning intestinal disease, the mechanisms by which stress influences intestinal pathophysiology in the weaned pig are not understood. The objectives of these experiments were to investigate the impact of weaning on gastrointestinal health in the pig and to assess the role of stress signaling pathways in this response. Nineteen-day-old pigs were weaned, and mucosal barrier function and ion transport were assessed in jejunal and colonic tissues mounted on Ussing chambers. Weaning caused marked disturbances in intestinal barrier function, as demonstrated by significant ( P < 0.01) reductions in transepithelial electrical resistance and increases in intestinal permeability to [3H]mannitol in both the jejunum and colon compared with intestinal tissues from age-matched, unweaned control pigs. Weaned intestinal tissues exhibited increased intestinal secretory activity, as demonstrated by elevated short-circuit current that was sensitive to treatment with tetrodotoxin and indomethacin, suggesting activation of enteric neural and prostaglandin synthesis pathways in weaned intestinal tissues. Western blot analyses of mucosal homogenates showed increased expression of corticotrophin-releasing factor (CRF) receptor 1 in the jejunum and colon of weaned intestinal tissues. Pretreatment of pigs with the CRF receptor antagonist α-helical CRF(9–41), which was injected intraperitoneally 30 min prior to weaning, abolished the stress-induced mucosal changes. Our results indicate that weaning stress induces mucosal dysfunction mediated by intestinal CRF receptors and activated by enteric nerves and prostanoid pathways.}, number={1}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Moeser, Adam J. and Klok, Carin Vander and Ryan, Kathleen A. and Wooten, Jenna G. and Little, Dianne and Cook, Vanessa L. and Blikslager, Anthony T.}, year={2007}, month={Jan}, pages={G173–G181} }
 @article{blikslager_yin_cochran_wooten_pettigrew_belknap_2006, title={Cyclooxygenase expression in the early stages of equine laminitis: A cytologic study}, volume={20}, DOI={10.1111/j.1939-1676.2006.tb00721.x}, abstractNote={Background:Recent reports indicate increased amounts of mRNA from inflammation‐related genes in the prodromal stage of laminitis.}, number={5}, journal={Journal of Veterinary Internal Medicine}, author={Blikslager, Anthony and Yin, C. L. and Cochran, A. M. and Wooten, J. G. and Pettigrew, A. and Belknap, J. K.}, year={2006}, pages={1191–1196} }
 @article{moeser_nighot_ryan_wooten_blikslager_2006, title={Prostaglandin-mediated inhibition of Na+/H+ exchanger isoform 2 stimulates recovery of barrier function in ischemia-injured intestine}, volume={291}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00380.2005}, DOI={10.1152/ajpgi.00380.2005}, abstractNote={Prostaglandins stimulate repair of the ischemia-injured intestinal barrier in the porcine ileum through a mechanism involving cAMP-dependent Cl−secretion and inhibition of electroneutral Na+/H+exchanger (NHE) activity. In the present study, we focused on the role of individual NHE isoforms in the recovery of barrier function. Ischemia-injured porcine ileal mucosa was mounted on Ussing chambers. Short-circuit current ( Isc), transepithelial electrical resistance (TER), and isotopic fluxes of22Na were measured in response to PGE2and selective inhibitors of epithelial NHE isoforms. Immunoassays were used to assess the expression of NHE isoforms. Forty-five minutes of intestinal ischemia resulted in a 45% reduction in TER ( P < 0.01). Near-complete restitution occurred within 60 min. Inhibition of NHE2 with HOE-694 (25 μM) added to the mucosal surface of the injured ileum stimulated significant elevations in TER, independent of changes in Iscand histological evidence of restitution. Pharmacological inhibition of NHE3 or NHE1 with mucosal S-3226 (20 μM) or serosal cariporide (25 μM), respectively, had no effect. Ischemia-injured tissues treated with mucosal S-3226 or HOE-694 exhibited equivalent reductions in mucosal-to-serosal fluxes of22Na+(by ∼35%) compared with nontreated ischemia-injured control tissues ( P < 0.05). Intestinal ischemia resulted in increased expression of the cytoplasmic NHE regulatory factor EBP50 in NHE2 but not in NHE3 immunoprecipitates. Selective inhibition of NHE2, and not NHE3, induces recovery of barrier function in the ischemia-injured intestine.}, number={5}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Moeser, Adam J. and Nighot, Prashant K. and Ryan, Kathleen A. and Wooten, Jenna G. and Blikslager, Anthony T.}, year={2006}, month={Nov}, pages={G885–G894} }