Neuroprotective Effects of Viral Overexpression of microRNA‐22 in Rat and Cell Models of Cerebral Ischemia‐Reperfusion Injury. Issue 2 (February 2015)

• Record Type: Journal Article
• Authors: Yu, Houyou; Wu, Mingchun; Zhao, Peng; Huang, Yang; Wang, Wei; Yin, Wen
• Is Part Of: Journal of cellular biochemistry. Volume 116:Issue 2(2015:Feb.)
• Page Start: 233
• Page End: 241
• Publication Date: 2015-02
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.24960
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>ABSTRACT</title> <sec id="jcb24960-sec-0001" sec-type="section"> <p>Several studies have reported that microRNA (MIR) is involved in the pathogenesis and progression of ischemic diseases, including cerebral ischemia, and that MIR‐22 may inhibit the inflammatory response and cell apoptosis, which contribute to ischemia/reperfusion (I/R) injury. However, the specific function of MIR‐22 in cerebral I/R injury remains far from clear. This study aimed to examine the potential protective effect of MIR‐22 against cerebral I/R injury and its mechanism. As predicted, adenovirus‐mediated MIR‐22 overexpression markedly reduced the neurological score and infarct size (<italic>P</italic> < 0.05). We demonstrated that MIR‐22 overexpression resulted in a reduction in inflammatory cytokines TNF‐α, IL‐6, COX‐2, and iNOS, whereas the level of IL‐10 was enhanced. MIR‐22 overexpression significantly inhibited NF‐κB activity by decreasing NF‐κB coactivator NCOA1 expression. Furthermore, we found that MIR‐22 could reduce the apoptotic rate of cortical neurons. Caspase‐3 activity was inhibited by MIR‐22, and the expression of the anti‐apoptosis gene Bcl‐2 in neurons was increased and that of the pro‐apoptosis gene Bax decreased following MIR‐22 overexpression. Our results suggest that MIR‐22 could be used to treat cerebral I/R injury and that its neuroprotective effect may be attributed to a reduction in inflammation and apoptosis. J. Cell. Biochem. 116: 233–241, 2015. © 2014 Wiley Periodicals, Inc.</p> </sec> </abstract>