Methylmercury alters proliferation, migration, and antioxidant capacity in human HTR8/SV-neo trophoblast cells

•The effects of methylmercury on first trimester trophoblast cells are examined.•1 μg/mL methylmercury inhibits proliferation and migration, and has many effects on antioxidant genes.•0.01 μg/mL and 0.1 μg/mL promote proliferation and decrease expression of a cell adhesion gene.•Trophoblast cells di...

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Published inReproductive toxicology (Elmsford, N.Y.) Vol. 78; pp. 60 - 68
Main Authors Tucker, Emily K., Nowak, Romana A.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.06.2018
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Summary:•The effects of methylmercury on first trimester trophoblast cells are examined.•1 μg/mL methylmercury inhibits proliferation and migration, and has many effects on antioxidant genes.•0.01 μg/mL and 0.1 μg/mL promote proliferation and decrease expression of a cell adhesion gene.•Trophoblast cells display unique responses to methylmercury in relation to neural cell lines. Methylmercury, a potent neurotoxin, is able to pass through the placenta, but its effects on the placenta itself have not been elucidated. Using an immortalized human trophoblast cell line, HTR8/SV-neo, we assessed the in vitro toxicity of methylmercury. We found that 1 μg/mL methylmercury decreased viability, proliferation, and migration; and it had effects on antioxidant genes similar to those seen in neural cells. However, methylmercury led to decreased expression of superoxide dismutase 1 and increased expression of surfactant protein D. HTR cells treated 0.01 or 0.1 μg/mL methylmercury had increased migration rates along with decreased expression of an adhesion gene, cadherin 3, suggesting that low doses of methylmercury promote migration in HTR cells. Our results indicate that trophoblast cells react differently to methylmercury relative to neural cell lines, and thus investigation of methylmercury toxicity in placental cells is needed to understand the effects of this heavy metal on the placenta.
ISSN:0890-6238
1873-1708
DOI:10.1016/j.reprotox.2018.03.008