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2017 ; 7
(1
): 16190
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Ischemic Postconditioning Protects Against Intestinal Ischemia/Reperfusion Injury
via the HIF-1?/miR-21 Axis
#MMPMID29170412
Jia Z
; Lian W
; Shi H
; Cao C
; Han S
; Wang K
; Li M
; Zhang X
Sci Rep
2017[Nov]; 7
(1
): 16190
PMID29170412
show ga
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-1?) 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-?, confirming the induction of miR-21 by HIF1-?, HIF1-? 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-?
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-? and the attenuation of apoptosis via the downregulation of PDCD4 and
Fas-L.
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