MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway
| العنوان: | MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway |
|---|---|
| المؤلفون: | Shijia Yu, Zhongqi Bu, Juan Feng, Mingjun Yu, Ping-Ping He |
| المصدر: | Neural Regeneration Research Neural Regeneration Research, Vol 16, Iss 6, Pp 1024-1030 (2021) |
| بيانات النشر: | Wolters Kluwer - Medknow, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | 0301 basic medicine, Programmed cell death, non-coding RNA, Ischemia, Pharmacology, lcsh:RC346-429, neurological function, apoptosis, cerebral ischemia and reperfusion injury, microrna, mir-670, neuron, non-coding rna, pathway, 03 medical and health sciences, chemistry.chemical_compound, miR-670, 0302 clinical medicine, Developmental Neuroscience, medicine, Antagomir, Artery occlusion, lcsh:Neurology. Diseases of the nervous system, microRNA, Cell growth, business.industry, Institutional Animal Care and Use Committee, medicine.disease, 030104 developmental biology, chemistry, Apoptosis, business, Reperfusion injury, 030217 neurology & neurosurgery, Research Article |
| الوصف: | 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). |
| اللغة: | English |
| تدمد: | 1876-7958 1673-5374 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1bfea0eeab3d582af80cabe10e645ad0Test http://europepmc.org/articles/PMC8224117Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....1bfea0eeab3d582af80cabe10e645ad0 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 18767958 16735374 |
|---|