Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

Abstract

RAS is involved in the pathophysiology of DSS-induced colitis and AT1a receptor may be a novel therapeutic target for the treatment of IBD.

Effects of the ACE2 inhibitor GL1001 on acute dextran sodium sulfate-induced colitis in mice

“…These findings are supported by recent animal data revealing an upregulation of Ang II and AT1 receptors in the colon of DSS-treated mice [31]. Other animal studies have demonstrated protective effects of ACE inhibition, AT1 receptor blockade, and AT1 receptor knockout in DSS and trinitrobenzene sulfonic acid models of colitis [31][32][33]. Together, these studies suggest that Ang II might in part mediate colonic inflammation in IBD via stimulation of the AT1 receptor.…”

“…For example, elevated levels of Ang I and Ang II have been found in colon tissue obtained from Crohn's disease patients, and the magnitude of elevation was associated with the degree of mucosal inflammation [29]. These findings are supported by recent animal data revealing an upregulation of Ang II and AT1 receptors in the colon of DSS-treated mice [31]. Other animal studies have demonstrated protective effects of ACE inhibition, AT1 receptor blockade, and AT1 receptor knockout in DSS and trinitrobenzene sulfonic acid models of colitis [31][32][33].…”

Positive cross talk between protein kinase D and β-catenin in intestinal epithelial cells: impact on β-catenin nuclear localization and phosphorylation at Ser552

“…In addition to its well-established role in the regulation of systemic blood pressure, ANG II is a regulatory peptide generated locally in the gastrointestinal tract that plays a role in gastrointestinal mucosal inflammation and carcinogenesis (20,24,76). Using ANG II to induce receptor-mediated PKD activation in IEC-18 cells (3,4,36,53,54), we produced several lines of evidence indicating that PKDs interact with endogenous ␤-catenin at multiple points in these cells.…”

Telmisartan attenuates the inflamed mesenteric adipose tissue in spontaneous colitis by mechanisms involving regulation of neurotensin/microRNA-155 pathway

“…In fact, increased expression of angiotensin II has been reported in experimental colitis [72] and patients with CD [73]. In addition, the renin-angiotensin system was reported to be involved in the pathophysiology of colitis, suggesting that antagonism of the renin-angiotensin system such as angiotensin II receptor may be a potential prophylactic strategy for the treatment of human IBD [74,75]. In fact, angiotensin receptor antagonist is effective in preventing experimental colitis through the blockade of growth factor-beta1 overexpression or via regulation of mucosal vascular addressin cell adhesion molecule 1 [76][77][78][79].…”