Upregulation of miR-20b-5p inhibits trophoblast invasion by blocking autophagy in recurrent miscarriage

Ruei Ci Lin, Yu Ying Chao, Mei Tsz Su, Hui Ling Tsai, Pei Yin Tsai, Chia Yih Wang

研究成果: Article同行評審

1 引文 斯高帕斯(Scopus)

摘要

Recurrent miscarriage is defined as more than three pregnancy failures occurring before 20 weeks of gestation. Poor differentiation of the endometrial stroma or defective trophoblast cell invasion at the maternal-fetal interface leads to recurrent miscarriages. Several miRNAs, including miR-20b-5p, are aberrantly regulated in recurrent miscarriages; however, the underlying molecular mechanisms remain unclear. Primary cilia are antenna-like organelles that coordinate signaling during development and differentiation. Defective primary cilia formation leads to complications, such as recurrent miscarriage or preeclampsia. Here, we demonstrated that miR-20b-5p inhibited trophoblast cell invasion by blocking primary cilia formation. Mechanistically, miR-20b-5p targeted and inhibited ATG16L1 and ATG7 expression, thereby blocking autophagy. Defective autophagy reduced primary cilia formation and stopped ERK activation, which is a crucial signaling pathway for trophoblast invasion. Aspirin is used to prevent recurrent miscarriages in clinical settings. Treatment with aspirin inhibited miR-20b-5p levels, thus restoring primary cilia formation and trophoblast invasion. Thus, our findings uncovered the molecular mechanism by which miR-20b-5p suppressed primary cilia formation and trophoblast invasion by reducing the expression of ATG16L1 and ATG7. Moreover, we found that the defective phenotypes could be rescued by aspirin in recurrent miscarriages.

原文English
文章編號110934
期刊Cellular Signalling
113
DOIs
出版狀態Published - 2024 1月

All Science Journal Classification (ASJC) codes

  • 細胞生物學

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