Pharmaceutical Activation or Genetic Absence of ClC-2 Alters Tight Junctions During Experimental Colitis

Inflammatory Bowel Diseases
Younggeon JinAnthony Blikslager

Abstract

We have previously reported that the ClC-2 chloride channel has an important role in regulation of tight junction barrier function during experimental colitis, and the pharmaceutical ClC-2 activator lubiprostone initiates intestinal barrier repair in ischemic-injured intestine. Thus, we hypothesized that pharmaceutical ClC-2 activation would have a protective and therapeutic effect in murine models of colitis, which would be absent in ClC-2 mice. We administered lubiprostone to wild-type or ClC-2 mice with dextran sulfate sodium (DSS) or 2, 4, 5-trinitrobenzene sulfonic acid-induced colitis. We determined the severity of colitis and assessed intestinal permeability. Selected tight junction proteins were analyzed by Western blotting and immunofluorescence/confocal microscopy, whereas proliferative and differentiated cells were examined with special staining and immunohistochemistry. Oral preventive or therapeutic administration of lubiprostone significantly reduced the severity of colitis and reduced intestinal permeability in both DSS and trinitrobenzene sulfonic acid-induced colitis. Preventive treatment with lubiprostone induced significant recovery of the expression and distribution of selected sealing tight junction protein...Continue Reading

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Citations

Dec 31, 2015·Tissue Barriers·Younggeon Jin, Anthony T Blikslager
Oct 5, 2018·American Journal of Physiology. Gastrointestinal and Liver Physiology·Younggeon JinAnthony T Blikslager
Apr 21, 2017·American Journal of Physiology. Cell Physiology·John CuppolettiDanuta H Malinowska
Feb 19, 2020·American Journal of Physiology. Gastrointestinal and Liver Physiology·Leandi KrügerAnthony T Blikslager
May 24, 2017·Molecular Medicine Reports·Hongwei WangXin Wang

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