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Mechanism of Na‐H Exchanger‐1 Expression in Experimental Colitis: Role of Carbonic Anhydrase
Author(s) -
Khan Islam,
AlShamali Amna
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.766.9
Subject(s) - colitis , gene isoform , carbonic anhydrase , western blot , chemistry , carbonic anhydrase ii , inflammatory bowel disease , medicine , enzyme , microbiology and biotechnology , biochemistry , biology , disease , gene
Na‐H exchanger‐1 (NHE‐1) plays an important role in the neutral uptake of NaCl and water from GI‐tract, and is suppressed in inflammatory bowel diseases (IBD). It is believed to be regulated by interaction of carbonic anhydrase (CA) with its C‐terminal domain. Therefore in this study we investigated a role of CA in experimental colitis induced in rats by intra‐rectal administration of trinitrobenzene sulphonic acid (TNBS). There are multiple CA isoforms which are expressed and regulated differently in various tissues. The isoforms CA‐I and ‐II are cytoplasmic while the CA‐IV is a membrane bound isoform. These isoforms are reported to express in the colon. In this study therefore we examined the level of CA isoforms ‐I, ‐II and ‐IV in colonic tissues taken from day 5 post colitis by western blot analysis. Colon was inflamed as indicated by elevation of MPO activity and tissue histology. There was suppression of protein levels of NHE‐1, CA‐1, ‐2 and ‐4 isoforms in the inflamed colon as compared to the non colitic controls. The levels of actin used as an internal control however remained unchanged in colitis. Since NHE‐1 is fueled by protons which are produced by CA, a concomitant suppression of CA expression in inflamed colon suggests that NHE‐1 is regulated by CA in colitis. Our findings discount the role of CA in contributing to an acidic pH of luminal contents reported in the IBD patients. Acknowledgment: A financial support from the Kuwait University is gratefully acknowledged.