The targeting of DAPK1 with miR‐190a‐3p promotes autophagy in trophoblast cells

Author:

Luo Qi‐qi12,Tian Yu1,Qu Guang‐jin1,Huang Kun13,Hu Pan‐pan1,Xue Ying1,Hu Bi‐feng4,Luo Shan‐shun1ORCID

Affiliation:

1. Department of Gerontology First Affiliated Hospital of Harbin Medical University Harbin People's Republic of China

2. Department of Cardiovascular Medicine, Army Characteristic Medical Center of PLA Da ping Hospital Chongqing People's Republic of China

3. Department of Gerontology The First Hospital of Jiaxing Jiaxing People's Republic of China

4. Department of Neurology, Army Characteristic Medical Center of PLA Da ping Hospital Chongqing People's Republic of China

Abstract

AbstractPre‐eclampsia (PE) is a dangerous pathological status that occurs during pregnancy and is a leading reason for both maternal and fetal death. Autophagy is necessary for cellular survival in the face of environmental stress as well as cellular homeostasis and energy management. Aberrant microRNA (miRNA) expression is crucial in the pathophysiology of PE. Although studies have shown that miRNA (miR)‐190a‐3p function is tissue‐specific, the precise involvement of miR‐190a‐3p in PE has yet to be determined. We discovered that miR‐190a‐3p was significantly lower and death‐associated protein kinase 1 (DAPK1) was significantly higher in PE placental tissues compared to normal tissues, which is consistent with the results in cells. The luciferase analyses demonstrated the target‐regulatory relationship between miR‐190a‐3p and DAPK1. The inhibitory effect of miR‐190a‐3p on autophagy was reversed by co‐transfection of si‐DAPK1 and miR‐190a‐3p inhibitors. Thus, our data indicate that the hypoxia‐dependent miR‐190a‐3p/DAPK1 regulatory pathway is implicated in the development and progression of PE by promoting autophagy in trophoblast cells.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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