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Mediators of Inflammation
Volume 2014, Article ID 901530, 11 pages
Research Article

Intestinal Mucosal Barrier Is Injured by BMP2/4 via Activation of NF-B Signals after Ischemic Reperfusion

1Department of General Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China
2Center of Medical Experiment & Technology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China
3Department of Surgery, University of Michigan, Ann Arbor, MI 48109, USA

Received 24 February 2014; Accepted 25 June 2014; Published 16 July 2014

Academic Editor: H. Barbaros Oral

Copyright © 2014 Kang Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Intestinal ischemic reperfusion (I/R) can cause dysfunction of the intestinal mucosal barrier; however, the mechanism of the intestinal mucosal barrier dysfunction caused by I/R remains unclear. In this study, using intestinal epithelial cells under anaerobic cultivation and an in vivo rat intestinal I/R model, we found that hypoxia and I/R increased the expression of BMP2/4 and upregulated BMP type Ia receptor and BMP type II receptor expression. We also found that exogenous BMP2/4 can activate the ERK and AKT signaling pathways in rat small intestine (IEC-6) cells, thereby activating NF-B signaling, which leads to increased levels of inflammatory factors, such as TNF- and IL-6. Furthermore, recombinant BMP2/4 decreased the expression of the tight junction protein occludin via the activation of the NF-B pathway; these effects were abolished by treatment with the BMP-specific antagonist noggin or the NF-B inhibitor pyrrolidine dithiocarbamate (PDTC). All these factors can destroy the intestinal mucosal barrier, thereby leading to weaker barrier function. On the basis of these data, we conclude that BMP2/4 may act as the pathogenic basis for intestinal mucosal barrier dysfunction when the intestines suffer an I/R injury. Our results provide background for the development pharmacologic interventions in the management of I/R injury.