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Issue 6, 2016
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Signals involved in the effects of bisphenol A (BPA) on proliferation and motility of Leydig cells: a comparative proteomic analysis

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Abstract

Recent studies indicated that bisphenol A (BPA) can disrupt spermatogenesis and then cause male infertility. The present study revealed that BPA greater than 10−6 M inhibited the proliferation of Leydig TM3 cells via a concentration dependent manner. The proteomic study revealed that 50 proteins were modulated in TM3 cells following exposure to BPA, which was relevant to structure, motility, cell metabolism, protein and nucleotide processing, and cell proliferation. Furthermore, BPA increased the in vitro migration and invasion of Leydig TM3 cells, which might be due to the BPA's modulation of proteins related to cell structure and motility such as actin and heat shock protein (HSP). Silencing of galectin-1, which was up regulated by BPA, significantly abolished the BPA-induced migration of TM3 cells. BPA treatment obviously increased the phosphorylation of ERK1/2 and Akt, while only PD98509 (ERK1/2 inhibitor) significantly attenuated BPA induced up regulation of galectin-1. Furthermore, PD98509 also reversed BPA induced migration of TM3 cells. Our study demonstrated that xenoestrogen BPA at micromolar or greater concentrations can modulate protein profiles, inhibit cell proliferation, and promote the in vitro migration and invasion of Leydig TM3 cells. It provided new insight into the mechanisms responsible for BPA induced male infertility.

Graphical abstract: Signals involved in the effects of bisphenol A (BPA) on proliferation and motility of Leydig cells: a comparative proteomic analysis

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Publication details

The article was received on 12 Jun 2016, accepted on 12 Sep 2016 and first published on 13 Sep 2016


Article type: Paper
DOI: 10.1039/C6TX00258G
Citation: Toxicol. Res., 2016,5, 1573-1584
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    Signals involved in the effects of bisphenol A (BPA) on proliferation and motility of Leydig cells: a comparative proteomic analysis

    Z. Chen, K. Zhang, L. Ge, H. Liu, L. Chen, J. Du and H. Wang, Toxicol. Res., 2016, 5, 1573
    DOI: 10.1039/C6TX00258G

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