Over-expression of stomatin causes syncytium formation in nonfusogenic JEG-3 choriocarcinoma placental cells

Tung Wei Chen, Hong Wen Liu, Yi Jia Liou, Jui Hao Lee, Chi Hung Lin*

*Corresponding author for this work

研究成果: Article

4 引文 斯高帕斯(Scopus)

摘要

Placental trophoblast differentiation involves the continuous fusion of mononuclear cytotrophoblasts. However, except for syncytin, little is known about the detailed mechanisms underlying trophoblast fusion. A previous study indicated that lipid rafts play an important role in HTLV-1 syncytium formation. To identify proteins that may be involved in placental trophoblast differentiation, we examined stomatin, an important lipid-raft protein that localizes to detergent-resistant membrane domains. The syncytium and human chorionic gonadotropin (β-hCG; a marker of placental trophoblast differentiation) were visualized by immunofluorescence staining. We found that overexpression of stomatin in the nonfusogenic JEG-3 cell line caused syncytium formation and increased the fusion index of cells. Treating these cells with N6,2′-O-dibutyryladenosine 3′,5′-cyclic monophosphate further increased cell fusion by stomatin. β-hCG was found in a few JEG-3 cells overexpressing stomatin at 48 h, and its levels increased dramatically at 72 h along with the formation of the multinuclear syncytium. RNA interference was used to decrease stomatin expression in BeWo cells, a fusogenic human choriocarcinoma cell line. After knockdown for 72 h, stomatin levels decreased by almost 95%. The fusion indexes of control and stomatin-knockdown cells at 72 h were 9.4 and 6.5%, respectively. Our data indicated that stomatin could trigger syncytium formation and upregulate β-hCG for cell fusion in nonfusogenic JEG-3 cells. Downregulation of stomatin slightly inhibited the fusion index of fusogenic BeWo cells. Thus, these data suggested that stomatin plays an important role in trophoblast differentiation.

原文English
頁(從 - 到)926-933
頁數8
期刊Cell Biology International
40
發行號8
DOIs
出版狀態Published - 1 八月 2016

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