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TGF‐β1 up‐regulates connexin43 expression: A potential mechanism for human trophoblast cell differentiation
Author(s) -
Cheng JungChien,
Chang HsunMing,
Fang Lanlan,
Sun YingPu,
Leung Peter C.K.
Publication year - 2015
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24902
Subject(s) - trophoblast , microbiology and biotechnology , syncytiotrophoblast , smad , transforming growth factor , gene knockdown , intracellular , signal transduction , cellular differentiation , downregulation and upregulation , biology , cell culture , chemistry , placenta , gene , genetics , fetus , pregnancy
Connexin43 (Cx43)‐mediated gap junctional intercellular communication (GJIC) are required for human trophoblast differentiation. To date, whether Cx43 mediates TGF‐β1‐induced trophoblast differentiation has not been determined. We showed that treatment with TGF‐β1 increased Cx43 expression and GJIC in HTR‐8/SVneo human trophoblast cells. In addition, Smad and ERK1/2 signaling pathways were involved in TGF‐β1‐induced up‐regulation of Cx43. Moreover, TGF‐β1 increased the expression of the syncytiotrophoblast marker, β‐hCG. Importantly, knockdown of Cx43 abolished the TGF‐β1‐induced up‐regulation of β‐hCG. Furthermore, overexpression of Cx43 up‐regulated β‐hCG expression. These results provide evidence that Cx43 and GJIC activity are up‐regulated by TGF‐β1 in human trophoblast cells, which subsequently contributes to TGF‐β1‐induced trophoblast differentiation. J. Cell. Physiol. 230: 1558–1566, 2015. © 2015 Wiley Periodicals, Inc., A Wiley Company