Molecular mechanisms of somatostatin-mediated intestinal epithelial barrier function restoration by upregulating claudin-4 in mice with DSS-induced colitis

American Journal of Physiology. Cell Physiology
Lin CaiChunhui Wang

Abstract

Intestinal barrier dysfunction plays a crucial role in the pathogenesis of ulcerative colitis (UC). Previous studies have shown somatostatin (SST) can protect intestinal barrier structure possibly through upregulating tight junction (TJ) protein expression, but the mechanisms of this upregulation remain undefined. This study aimed to investigate the molecular mechanisms of interaction of SST with its downstream regulatory elements in DSS-induced colitis mice. In DSS-induced colitis mice, exogenous SST supplement (octreotide) effectively ameliorated disease progression, restored colonic barrier structure and function, and stimulated claudin-4 expression. Similar effects were also observed for SST on Caco-2 cells intervened by TNF-α. SST receptor 5 (SSTR5) agonist L-817,818 upregulated the claudin-4 expression whereas the SSTR2 agonist seglitide could not reverse TNF-α-induced reduction of claudin-4. SST treatment significantly decreased the phosphorylation levels of ERK1/2 and p38 induced by TNF-α. PD-98059 (ERK1/2 pathway inhibitor) but not SB-202190 (p38 pathway inhibitor) could reverse TNF-α-induced suppression of claudin-4 expression. Both inhibitors could improve the TJ barrier function damaged by TNF-α. Our studies suggest...Continue Reading

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Methods Mentioned

BETA
transmission electron microscopy
PCR
reverse-transcription PCR

Software Mentioned

SPSS

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