Down-regulating microRNA-20a regulates CDH1 to protect against cerebral ischemia/reperfusion injury in rats. Issue 1 (2nd January 2021)

• Record Type: Journal Article
• Authors: Yang, Chun-chun; Wei, Xiang-pin; Fu, Xian-ming; Qian, Ling-tao; Xie, Lan-jun; Liu, Hong-bo; Li, Gang; Li, Xin-gang; Zeng, Xian-wei
• Is Part Of: Cell cycle. Volume 20:Issue 1(2021)
• Page Start: 54
• Page End: 64
• Publication Date: 2021-01-02
• Subjects: Cerebral ischemia/reperfusion injury -- microRNA-20a -- cadherin-1 -- pathological damage -- nerve injury -- oxidative stress; Cell cycle -- Periodicals; 571.84377
• DOI: 10.1080/15384101.2020.1856498
• Languages: English
• ISSNs: 1538-4101

Abstract

ABSTRACT: Studies have extensively focused on the involvement of microRNAs (miRNAs) in cerebral ischemia/reperfusion (I/R) injury but not much on the specific role of miR-20a. Hence, this study is purposed to decipher whether miR-20a could regulate cadherin 1 (CDH1) to affect cerebral I/R injury in rats. Rat transient middle cerebral artery occlusion model (MCAO) was established. Rats were injected with lentiviral solution containing miR-20a inhibitor, or overexpressed CDH1 or combined depleted miR-20a and CDH1 to explore their roles in cerebral I/R injury. Oxidative stress-related factors, miR-20a, CDH1, nuclear factor-kappaB (NF-κB) and Nestin expression in brain tissues were detected by RT-qPCR and western blot assay. The target relation between miR-20a and CDH1 was predicted by online website and further confirmed by luciferase activity assay. In rats with cerebral I/R injury, increased miR-20a and decreased CDH1 were found in brain tissues. Reduction of miR-20a or elevation of CDH1 attenuated behavior function in MCAO rats. Inhibiting miR-20a or restoring CDH1 restrained oxidative stress, attenuated pathological damage of neurons, promoted neuron survival, and down-regulated NF-κB and Nestin expression in brain tissues of MCAO rats. CDH1 was determined to a target gene of miR-20a. This study elucidates that down-regulating miR-20a elevates CDH1 to protect neurons from cerebral I/R injury, which paves a new way for treatment of cerebral I/R injury.