Next Article in Journal
Interactions between Triterpenes and a P-I Type Snake Venom Metalloproteinase: Molecular Simulations and Experiments
Previous Article in Journal
Comment on Ultrasound Guidance for Botulinum Neurotoxin Chemodenervation Procedures. Toxins 2017, 10, 18—Quintessential Use of Ultrasound Guidance for Botulinum Toxin Injections—Muscle Innervation Zone Targeting Revisited
Article Menu

Export Article

Open AccessArticle
Toxins 2018, 10(10), 398; https://doi.org/10.3390/toxins10100398

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

1
College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China
2
Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China
3
Joint International Research Laboratory of Agriculture and Agri-Product Safety, the Ministry of Education of China, Yangzhou University, Yangzhou 225009, China
*
Author to whom correspondence should be addressed.
Received: 1 September 2018 / Revised: 16 September 2018 / Accepted: 19 September 2018 / Published: 28 September 2018
(This article belongs to the Section Mycotoxins)
Full-Text   |   PDF [3807 KB, uploaded 28 September 2018]   |  

Abstract

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. View Full-Text
Keywords: Zearalenone (ZEA); Sertoli cells (SCs); cell cycle; G2/M arrest; Autophagy; PI3K/Akt/m TOR signaling Zearalenone (ZEA); Sertoli cells (SCs); cell cycle; G2/M arrest; Autophagy; PI3K/Akt/m TOR signaling
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Wang, B.-J.; Zheng, W.-L.; Feng, N.-N.; Wang, T.; Zou, H.; Gu, J.-H.; Yuan, Y.; Liu, X.-Z.; Liu, Z.-P.; Bian, J.-C. 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 2018, 10, 398.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Toxins EISSN 2072-6651 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top