TGF-β1 alleviates HgCl2 induced apoptosis via P38 MAPK signaling pathway in human trophoblast cells.

It is well known that embryonic development can be perturbed by environmental factors such as heavy metals. Mercury is one of the most significant threats to the environment and human health. Mercury can damage many parts of the human body, including lungs, kidneys, nerves and fetus. However, the effect of mercury on human embryo remains unknown. Here, we showed that HgCl2 treatment resulted in a significant increase in apoptosis in HTR-8/SVneo cells. However, the effect of HgCl2 on apoptosis was partially reduced by the combination treatment with TGF-β1 and HgCl2 in HTR-8/SVneo cells. Moreover, HgCl2 treatment gradually decreased the expression of TGF-β1 in a dose dependent manner. Furthermore, a P38 MAPK inhibitor, SB202190, decreased the cell apoptosis and caspase activation induced by HgCl2 in trophoblast cells. In addition, TGF-β1 alleviated HgCl2 induced apoptosis of HTR-8/SVneo cells via p38 MAPK signaling pathway, which was involved in the TAK1 expression. These results might provide a theoretical basis for mercury induced trophoblast associated embryo damage and a potential avenue of intervention.