Relevance of Wnt10b and activation of β‐catenin/ GCM a/syncytin‐1 pathway in BeWo cell fusion

Problem To study the involvement of specific Wnt(s) ligand during trophoblastic BeWo cell differentiation. Method of study BeWo cells on treatment with forskolin/human chorionic gonadotropin ( hCG ) were studied for cell fusion by desmoplakin I+II staining and/or hCG secretion by ELISA . Levels of Wnt10b/β‐catenin/glial cell missing a ( GCM a)/syncytin‐1 were studied by qPCR /Western blotting in forskolin‐/ hCG ‐treated control si RNA and Wnt10b silenced BeWo cells. Results BeWo cells on treatment with hCG (5  IU / mL ) led to a 94‐fold increase in Wnt10b transcript. Wnt10b silencing showed significant decrease in forskolin‐/ hCG ‐mediated BeWo cell fusion and/or hCG secretion. It led to down‐regulation of β‐catenin (nuclear and cytoplasmic), GCM a and syncytin‐1 expression. Treatment of BeWo cells with H89, protein kinase A ( PKA ) signaling inhibitor, significantly reduced forskolin‐/ hCG ‐induced Wnt10b, β‐catenin, and syncytin‐1 expression, which also resulted in reduced cell fusion. Conclusion Wnt10b is involved in forskolin/ hCG ‐mediated BeWo cell fusion via β‐catenin/ GCM a/syncytin pathway, which may also involve activation of PKA .