1a:I[76865,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"Grid"] 1b:I[17291,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"GridCol"] 1c:I[34616,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"Avatar"] 1d:I[32972,["/_next/static/chunks/d07a36b34c614bac.js","/_next/static/chunks/a439560253821848.js","/_next/static/chunks/992d80515d7f780d.js","/_next/static/chunks/3adfb55b15c8d19c.js","/_next/static/chunks/b642b3e65e2c6231.js","/_next/static/chunks/fc50eca1ad01dc11.js","/_next/static/chunks/afc6bdd59b458409.js","/_next/static/chunks/6448cccc5d968256.js"],"default"] 1e:T4a1,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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