The Effects of Autophagy and PI3K/AKT/m-TOR Signaling Pathway on the Cell-Cycle Arrest of Rats Primary Sertoli Cells Induced by Zearalenone

Toxins

Bing-jie Wang¹  Hui Zou¹  Tao Wang¹  Yan Yuan¹  Xue-zhong Liu¹  Wang-long Zheng¹  Jian-hong Gu¹  Zong-ping Liu¹  Nan-nan Feng¹  Jian-chun Bian¹ 

[1] College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China;

关键词: Zearalenone (ZEA);    Sertoli cells (SCs);    cell cycle;    G2/M arrest;    Autophagy;    PI3K/Akt/m TOR signaling;   

DOI  :  10.3390/toxins10100398

来源: DOAJ

【 摘 要 】

A high concentration of Zearalenone (ZEA) will perturb the differentiation of germ cells, and induce a death of germ cells, but the toxic mechanism and molecular mechanism remain unclear. The Sertoli cells (SCs) play an irreplaceable role in spermatogenesis. In order to explore the potential mechanism of ZEA male reproductive toxicity, we studied the effects of ZEA on cell proliferation, cell-cycle distribution, cell-cycle-related proteins and autophagy-related pathway the PI3K/Akt/mTOR signaling in primary cultured rats SCs, and the effects of autophagy and PI3K/AKT/m TOR signaling pathway on the SCs cell-cycle arrest induced by ZEA treated with the autophagy promoter RAPA, autophagy inhibitor CQ, and the PI3K inhibitor LY294002, respectively. The data revealed that ZEA could inhibit the proliferation of SCs by arresting the cell cycle in the G2/M phase and trigger the autophagy via inhibiting the PI3K/Akt/m TOR signaling pathway. Promoting or inhibiting the level of autophagy could either augment or reverse the arrest of cell cycle. And it was regulated by PI3K/Akt/m TOR signaling pathway. Taken together, this study provides evidence that autophagy and PI3K/Akt/m TOR signaling pathway are involved in regulating rats primary SCs cell-cycle arrest due to ZEA in vitro. To some extent, ZEA-induced autophagy plays a protective role in this process.

【 授权许可】

Unknown