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Theriogenology

Title:		The role of ALOX15B in heat stress-induced apoptosis of porcine sertoli cells
Author(s):		Xue H; Huo Y; Hu Y; Zhang J; Deng C; Zhang J; Wang X;
Address:		"Chongqing Key Laboratory of Forage & Herbivore, College of Veterinary Medicine, Southwest University, Beibei, Chongqing, 400715, PR China. Chongqing Key Laboratory of Forage & Herbivore, College of Veterinary Medicine, Southwest University, Beibei, Chongqing, 400715, PR China. Electronic address: wang1973@swu.edu.cn"
Journal Title:		Theriogenology
Year:		2022
Volume:		20220319
Issue:
Page Number:		6 - 15
DOI:		10.1016/j.theriogenology.2022.03.018
ISSN/ISBN:		1879-3231 (Electronic) 0093-691X (Linking)
Abstract:		"Heat stress reduces the number of Sertoli cells and impairs spermatogenesis. Mounting evidence indicates that lipid homeostasis is fundamental to cell survival. However, little is known about the role of lipid peroxides in the heat stress-induced apoptosis of Sertoli cells. In the present study, we used metabolomics to explore the changes of lipid peroxides in porcine Sertoli cells under heat stress using liquid chromatograph-mass spectrometry. These results showed a notable increase in the content of 8-hydroxyeicosatetraenoic acid (8-HETE), and 15-hydroxyeicosatetraenoic acid (15-HETE). Furthermore, we found that among arachidonate lipoxygenases, heat stress significantly increased the expression of arachidonate 15-lipoxygenase type B (ALOX15B). Moreover, baicalein, a specific inhibitor of ALOX15B, reduced the content of 8-HETE and 15-HETE, and decreased the apoptosis rate in heat stress-treated porcine Sertoli cells. In addition, baicalein and small interfering RNAs targeting ALOX15B increased the content of 8-HETE and 15-HETE, and activated the p38-p53 pathway, causing apoptosis in heat stress treated porcine Sertoli cells. Interestingly, a p38 inhibitor decreased the expression of ALOX15B, reduced the content of 8-HETE and 15-HETE, and decreased the expression of p53 and the apoptosis rate in heat stress treated porcine Sertoli cells. A p53 inhibitor had similar effect on Sertoli cells. These results indicated that heat stress enhanced the expression of ALOX15B, increased the content of 8-HETE and 15-HETE, and activated the p38-p53 pathway to cause apoptosis. ALOX15B and lipid peroxides obtained feedback from the p38-p53 pathway. Our findings will help to reveal the mechanism of lipid metabolism in Sertoli cells, and could provide a new targeted substrate for anti-heat stress strategies"
Keywords:		Animals Apoptosis Heat-Shock Response *Lipid Peroxides/pharmacology Male *Sertoli Cells Swine Tumor Suppressor Protein p53 Alox15b Heat stress Sertoli cells;
Notes:		"MedlineXue, Hongyan Huo, Yuannan Hu, Yu Zhang, Jinlong Deng, Chengchen Zhang, Jiaojiao Wang, Xianzhong eng 2022/03/29 Theriogenology. 2022 Jun; 185:6-15. doi: 10.1016/j.theriogenology.2022.03.018. Epub 2022 Mar 19"