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Mir-96-5p and mir-101-3p as potential intervention targets to rescue TiO2 NPs induced autophagy and migration impairment of human trophoblastic cells

Abstract

Autophagy induced by titanium dioxide nanoparticles (TiO2 NPs) had been realized nowadays, but the underlying mechanisms remains largely unknown. Animal studies had confirmed that autophagy might be an important mechanism to impair placenta, while how to reverse the damage were not clear. Here we used human HTR-8/SVneo (HTR) cells as a proper model to explore how autophagy was regulated in TiO2 NPs exposed human placenta cells. Our studies showed that TiO2 NPs could enter HTR cells and locate in cytoplasm, though they didn’t affect cell viability even under 100μg/ml, autophagy was observed and cell migration ability was severely impaired. Further study showed that TiO2 NPs increased the expression of both miR-96-5p and miR-101-3p, and then they targeted mTOR and decreased the expression of mTOR proteins. In addition, miR-96-5p also targeted Bcl-2 to down-regulated Bcl-2 protein level, which was also a key regulator of autophagy. We proved that when two microRNAs inhibitors were added, cell autophagy was, to a greater extent, reversed compared with one inhibitor was added, and the cell migration ability also reversed in more degree. Our studies revealed that TiO2 NPs might impair placenta development via autophagy. And mir-96-5p, as well as mir-101-3p, may choose as potential targets to reverse TiO2 NPs induced autophagy and placenta dysfunction.

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Publication details

The article was received on 24 Jul 2018, accepted on 02 Oct 2018 and first published on 03 Oct 2018


Article type: Paper
DOI: 10.1039/C8BM00856F
Citation: Biomater. Sci., 2018, Accepted Manuscript
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    Mir-96-5p and mir-101-3p as potential intervention targets to rescue TiO2 NPs induced autophagy and migration impairment of human trophoblastic cells

    Z. Mao, M. Yao, Y. Li, Z. Fu, S. Li, L. Zhang, Z. Zhou, Q. Tang, X. Han and Y. Xia, Biomater. Sci., 2018, Accepted Manuscript , DOI: 10.1039/C8BM00856F

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