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Ischemic Postconditioning Protects Against Intestinal Ischemia/Reperfusion Injury via the HIF-1a/miR-21 Axis.

Authors: Jia, Zhongzhi  Lian, Weishuai  Shi, Haifeng  Cao, Chuanwu  Han, Shilong  Wang, Kai  Li, Maoquan  Zhang, Xiaoping 
Citation: Jia Z, etal., Sci Rep. 2017 Nov 23;7(1):16190. doi: 10.1038/s41598-017-16366-6.
Pubmed: (View Article at PubMed) PMID:29170412
DOI: Full-text: DOI:10.1038/s41598-017-16366-6

Intestinal ischemia/reperfusion (I/R) can lead to tissue damage associated with inflammation and mucosal apoptosis. Ischemic postconditioning (IPostC), a series of repeated, brief, intermittent periods of ischemia and reperfusion, has beneficial effects against I/R-induced injury in the heart and intestine, although the underlying mechanisms for these effects remain unclear. We evaluated the involvement of microRNA-21 (miR-21) in the protective effects of IPostC in a rat model of I/R induced by superior mesenteric artery occlusion and reopening. IPostC decreased I/R injury and suppressed apoptosis in the intestinal tissues concomitant with the induction of hypoxia inducible factor 1 alpha (HIF-1α) and the upregulation of miR-21. In vitro experiments in the intestinal epithelial cell line IEC-6 showed that hypoxia induced miR-21 and this effect was abolished by silencing HIF1-α, confirming the induction of miR-21 by HIF1-α, HIF1-α or miR-21 inhibition exacerbated I/R induced apoptosis, and programmed cell death 4 (PDCD4) and Fas-L was involved in miR-21 mediated anti-apoptotic effects on intestinal epithelial cells. Knockdown of miR-21 or inhibition of HIF1-α abolished the IPostC-mediated attenuation of intestinal injury and apoptosis and the downregulation of PDCD4 and Fas-L. A potential mechanism underlying the protective effect of IPostC may therefore involve the induction of miR-21 by HIF1-α and the attenuation of apoptosis via the downregulation of PDCD4 and Fas-L.

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RGD Object Information
RGD ID: 13792603
Created: 2018-09-17
Species: All species
Last Modified: 2018-09-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.