热休克蛋白
热休克蛋白70
卵巢
生物
热应力
基因
热休克蛋白90
细胞生物学
内科学
内分泌学
男科
医学
遗传学
动物科学
作者
Mingyan Bei,Qian Wang,Wensai Yu,Lu Han,Jing Yu
标识
DOI:10.1016/j.jtherbio.2020.102532
摘要
Heat stress reduces oocyte competence, thereby causing lower fertility in animals. Chronic and acute heat stresses cause extensive morphological damage in animals, but few reports have focused on the effects of chronic and acute heat stresses on ovarian function and heat shock protein (HSP) gene expression during ovarian injury. In this study, we subjected female mice to chronic and acute heat stresses; we then calculated the ovary index, examined ovary microstructure, and measured the expression of multiple HSP family genes. Chronic heat stress reduced whole-body and ovarian growth but had little effect on the ovarian index; acute heat stress did not alter whole-body or ovarian weight. Both chronic and acute heat stresses impaired ovary function by causing the dysfunction of granular cells. Small HSP genes increased rapidly after heat treatment, and members of the HSP40, HSP70, and HSP90 families were co-expressed to function in the regulation of the heat stress response. We suggest that the HSP chaperone machinery may regulate the response to heat stress in the mouse ovary.
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