miR-181a regulates mitophagy and improves cognitive function in vascular dementia via targeting PINK1/Parkin pathway

Author:

Li Xiuqin1,Chen Shaopeng2,Wang Suxing3,Bai Xuedong3,Lv Peiyuan1

Affiliation:

1. Department of Neurology, Hebei Medical University, Shijiazhuang, Hebei, 050000, China

2. Department of Preventive Health, Hebei General Hospital, Shijiazhuang, Hebei, 050000, China

3. Department of Geriatrics, Hebei General Hospital, Shijiazhuang, Hebei, 050000, China

Abstract

This study investigates the mechanism of miR-181a in cognitive function and mitophagy in vascular dementia. A rat model of vascular dementia was established by common carotid artery ligation and then divided into model group (n= 10), mimics group (n= 10), inhibitors group (n= 10), NC group (n= 10), and the remaining 10 rats were in sham operation group. The rats in mimics group were intravenously injected with miR-181a mimics and rats in inhibitors group were injected with miR-181a inhibitors. Model group and mimics group rats had a longer time on the 3rd to 4th day than sham operation group, and inhibitors group had a shorter time than model group and mimics group (allP<0.05). Time in quadrant of the cylindrical platform in model group and mimics group was shortened while it was prolonged in inhibitors group (P< 0.05). miR-181a mRNA level in model group, inhibitors group and NC group was lower. On the contrary, PINK1 and Parkin level was higher. miR-181a mRNA level was higher in mimics group with lower levels of PINK1 and Parkin (P<0.05). miR-181a level in mimics group was significantly increased and PINK1 and Parkin mRNA was decreased. miR-181a mRNA level in inhibitors group decreased significantly, while PINK1 and Parkin mRNA was increased (P<0.05). Parkin expression in mimics group and NC group was reduced. Up-regulation of miR-181 (mimics group) can target and inhibit PINK1/Parkin mRNA, thereby inhibiting mitophagy. miR-181a downregulation in mitochondria can promote PINK1/Parkin expression, thereby activating mitophagy in rats with vascular dementia, alleviating mitochondrial dysfunction, and improving the cognitive ability of rats.

Publisher

American Scientific Publishers

Subject

General Materials Science

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