期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 10, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2022.852561
关键词
syncytin; placental angiogenesis; syncytiotrophoblast; pathological placenta; PI3K; Akt; mTOR pathway
In this study, we found that syncytin participates in angiogenesis during placental development, as observed in mice with an inducible syncytin-a gene knockout. We also found that syncytin affects the expression of vascular endothelial growth factor, placental growth factor, and soluble fms-like protein kinase-1, as well as the PI3K/Akt/mTOR pathway and the ability to induce tube formation by HUVECs. This new insight into syncytin and the pathophysiology of placenta-related diseases such as fetal growth restriction is significant.
Background: Syncytin, a retroviral envelope protein, is specifically expressed on trophoblast cells and mediates formation of the syncytiotrophoblast through fusogenic activity. Decreased expression of Syncytin was found in fetal growth restriction placentas.Results: By generating an inducible knockout of the syncytin-a gene in mice, we show a specific disruption of placental angiogenesis with abnormal formation of two syncytiotrophoblast layers. Consistent with the defects observed in vivo, conditioned medium collected from trophoblast cells, following Syncytin-1 knockdown, contains lower expression of vascular endothelial growth factor and placental growth factor, and higher levels of soluble fms-like protein kinase-1 in BeWo and HTR-8/SVneo cells which related with suppressed PI3K/Akt/mTOR pathway, and is reduced in ability to induce tube formation by HUVECs.Conclusion: Syncytin participates in angiogenesis during placental development was first identified both in vivo and in vitro. Here, we give a new sight on understanding syncytin and pathophysiology of placenta related disease such as fetal growth restriction.
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