Evidence for tight junction protein disruption in intestinal mucosa of malignant obstructive jaundice patients

Abstract

TJs in MOJ patients with jaundice were disrupted in the intestinal epithelium, which may have resulted from the alterations in TJ-related protein expression. TJ interruption may be a key factor contributing to intestinal mucosal barrier injury and increased intestinal permeability.

Histidine Decarboxylase Is Identified as a Potential Biomarker of Intestinal Mucosal Injury in Patients with Acute Intestinal Obstruction

“…Recently, several studies have revealed that TJPs including ZO-1, occludin and claudin-1, which are the essential components of the intestinal mucosal barrier, reflect the changes of intestinal mucosal function (56)(57)(58)(59), and thus the reduction of these proteins may indicate IMI. In the present study, the expression levels of D 1 7 ( 1 1 -1 2 ) 1 3 2 3 -1 3 3 7 , N ZO-1, occludin and claudin-1 were tested at both mRNA and protein levels by QRT-PCR, Western blotting and IHC in colonic mucosal tissues of STR-IO patients and in the adjacent "normal" colonic tissues of patients with colon cancer, to confirm the existence of IMI in patients with AIO, mainly STR-IO.…”

Curcumin Ameliorates Hydrogen Peroxide-Induced Epithelial Barrier Disruption by Upregulating Heme Oxygenase-1 Expression in Human Intestinal Epithelial Cells

“…Transmembrane proteins interact with other intracellular plaque proteins including zonula occludens (ZO-1, 2, and 3), which anchor the transmembrane proteins to the actin cytoskeleton [3,4]. A significant body of evidence indicates that disruption of TJ and increased paracellular permeability are crucially important in the pathogenesis of gastrointestinal disorders, for example inflammatory bowel disease (IBD), obstructive jaundice (OJ), acute pancreatitis (AP), alcohol-induced liver injury, among others [1,2,[5][6][7]. Oxidative stressinduced opening of the intestinal TJ barrier is an important mechanism contributing to the TJ barrier defect present in a variety of conditions of the gut [6,[8][9][10].…”

Pathogenesis of Inflammatory Bowel Diseases

“…At least 24 different claudin proteins are present in mammals , 2006, and these proteins are the primary component of tight junction strands (Furuse et al, 2006). Claudins are expressed in a tissue-specific manner, studies on human intestine confirm the expression of claudins-1, -2, -3, -4, -5, -7, and -8 in the colon, expression of claudins-1, -2, -3, and -4 in the duodenum, and expression of claudins-2 and -4 in the jejunum (Burgel et al, 2002;Escaffit et al, 2005, Szakal et al, 2010Wang et al, 2010;Zeissing et al, 2007). The molecular anatomy of transport through tight junction is not yet clear, at least two routes allow transport across the tight junction, and the relative contributions of different paracellular transport are regulated independently (Fihn et al, 2000;Van Itallie, 2008;Watson et al, 2005).…”