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Int J Biol Sci 2015; 11(6):664-671. doi:10.7150/ijbs.10783

Research Paper

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

Lihua Sun, Chao Xu, Guoqing Chen, Min Yu, Songwei Yang, Yuan Qiu, Ke Peng, Wensheng Wang, Weidong Xiao, Hua Yang

Department of General Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.


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.

Keywords: OS-9, intestinal epithelial barrier, p38, tight junction

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See for full terms and conditions.
How to cite this article:
Sun L, Xu C, Chen G, Yu M, Yang S, Qiu Y, Peng K, Wang W, Xiao W, Yang H. A Novel Role of OS-9 in the Maintenance of Intestinal Barrier Function from Hypoxia-induced Injury via p38-dependent Pathway. Int J Biol Sci 2015; 11(6):664-671. doi:10.7150/ijbs.10783. Available from