A Novel Role of OS-9 in the Maintenance of Intestinal Barrier Function from Hypoxia-induced Injury via p38-dependent Pathway.

A Novel Role of OS-9 in the Maintenance of Intestinal Barrier Function from Hypoxia-induced Injury via p38-dependent Pathway.
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OS-9 通过 p38 依赖性途径维持缺氧损伤肠屏障功能的新作用

DOI:
10.7150/ijbs.10783
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发表时间:
2015
影响因子:
9.2
通讯作者:
Yang H
Yang H
中科院分区:
生物学2区
文献类型:
--
作者:
Sun L;Xu C;Chen G;Yu M;Yang S;Qiu Y;Peng K;Wang W;Xiao W;Yang H

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OS-9 is a lectin required for efficient ubquitination of glycosylated substrates of endoplasmic reticulum-associated degradation (ERAD). OS-9 has previously been implicated in ER-to-Golgi transport and transcription factor turnover. However, we know very little about other functions of OS-9 under endoplasmic reticulum stress. Here, we used gene knockdown and overexpression approaches to study the protective effect of OS-9 on intestinal barrier function of intestinal epithelial cell Caco-2 monolayer. We found that OS-9 attenuated intestinal epithelial barrier dysfunction under hypoxia through up-regulating occludin and claudin-1 protein expression. Furthermore, we showed that the up-regulation of occludin and claudin-1 induced by OS-9 was mediated by p38 and ERK1/2 phosphorylation and did not involve HIF-1α. In summary, our results demonstrate that OS-9 up-regulates occludin and claudin-1 by activating the MAP kinase (MAPK) pathway, and thus protects the epithelial barrier function of Caco-2 monolayer under hypoxia condition.
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