MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway
Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury. MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury. However, whether miR-670 can regulate cell growth and...
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Wolters Kluwer Medknow Publications
2021-01-01
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doaj-d20923b900954489b98344a8daab956d2020-12-02T13:12:34ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742021-01-011661024103010.4103/1673-5374.300455MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathwayShi-Jia YuMing-Jun YuZhong-Qi BuPing-Ping HeJuan FengApoptosis is an important programmed cell death process involved in ischemia/reperfusion injury. MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury. However, whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood. In this study, we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo. Our results showed that after ischemia/reperfusion injury, miR-670 expression was obviously increased. After miR-670 expression was inhibited with an miR-670 antagomir, cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced. When miR-670 overexpression was induced by an miR-670 agomir, neuronal apoptosis was increased. In addition, we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits. Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury. These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway, which may be a potential target for treatment of cerebral ischemia/reperfusion injury. The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27, 2017 (IRB No. 2017PS035K).http://www.nrronline.org/article.asp?issn=1673-5374;year=2021;volume=16;issue=6;spage=1024;epage=1030;aulast=Yuapoptosis; cerebral ischemia and reperfusion injury; microrna; mir-670; neurological function; neuron; non-coding rna; pathway |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Shi-Jia Yu Ming-Jun Yu Zhong-Qi Bu Ping-Ping He Juan Feng |
spellingShingle |
Shi-Jia Yu Ming-Jun Yu Zhong-Qi Bu Ping-Ping He Juan Feng MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway Neural Regeneration Research apoptosis; cerebral ischemia and reperfusion injury; microrna; mir-670; neurological function; neuron; non-coding rna; pathway |
author_facet |
Shi-Jia Yu Ming-Jun Yu Zhong-Qi Bu Ping-Ping He Juan Feng |
author_sort |
Shi-Jia Yu |
title |
MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway |
title_short |
MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway |
title_full |
MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway |
title_fullStr |
MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway |
title_full_unstemmed |
MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway |
title_sort |
microrna-670 aggravates cerebral ischemia/reperfusion injury via the yap pathway |
publisher |
Wolters Kluwer Medknow Publications |
series |
Neural Regeneration Research |
issn |
1673-5374 |
publishDate |
2021-01-01 |
description |
Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury. MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury. However, whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood. In this study, we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo. Our results showed that after ischemia/reperfusion injury, miR-670 expression was obviously increased. After miR-670 expression was inhibited with an miR-670 antagomir, cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced. When miR-670 overexpression was induced by an miR-670 agomir, neuronal apoptosis was increased. In addition, we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits. Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury. These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway, which may be a potential target for treatment of cerebral ischemia/reperfusion injury. The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27, 2017 (IRB No. 2017PS035K). |
topic |
apoptosis; cerebral ischemia and reperfusion injury; microrna; mir-670; neurological function; neuron; non-coding rna; pathway |
url |
http://www.nrronline.org/article.asp?issn=1673-5374;year=2021;volume=16;issue=6;spage=1024;epage=1030;aulast=Yu |
work_keys_str_mv |
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