Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy.
Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy.
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前列腺素 F2 α 通过内质网应激和自噬诱导山羊黄体退化
DOI：
10.3389/fphys.2020.00868
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发表时间：
2020
影响因子：
4
通讯作者：
Jin Y
中科院分区：
文献类型：
--
作者：
Wen X;Liu L;Li S;Lin P;Chen H;Zhou D;Tang K;Wang A;Jin Y
黄体（CL）是哺乳动物产生孕酮维持妊娠的短暂内分泌组织。此外，CL的消退对于发情周期的开始是必要的。大量研究表明，前列腺素F2α（PGF 2 α）可诱导反刍动物CL的消退。然而，内质网应激和自噬在PGF 2 α诱导的山羊CL消退中的作用机制尚不清楚。本研究以间情期山羊和妊娠3个月山羊为研究对象，对ER应激相关蛋白GRP 78的定位进行了研究。通过Western blot分析证实了山羊CL发情周期中黄体期的不同阶段与ER应激相关蛋白和自噬相关蛋白表达变化之间的关系。结果表明，雌激素受体应激和自噬在山羊黄体晚期均被激活。为了揭示内质网应激和自噬在前列腺素F 2 α（PGF 2 α）诱导的CL消退过程中的作用，我们分别用4-苯基丁酸（4-PBA）和氯喹（CQ）抑制内质网应激和自噬。通过流式细胞仪检测细胞凋亡率和Western blotting检测ER应激和自噬相关蛋白的表达，证明ER应激促进了山羊黄体细胞凋亡和自噬，抑制自噬可以促进细胞凋亡。此外，敲低EIF 2S 1，阻断PERK通路的激活，通过减少PGF 2 α处理的山羊黄体细胞的自噬，促进细胞凋亡。本研究表明，ER应激通过促进山羊黄体细胞凋亡调节CL的消退，并通过激活自噬抑制山羊黄体细胞凋亡，其机制可能与PERK信号通路有关。
Corpus luteum (CL) is a transient endocrine tissue that produces progesterone for maintaining pregnancy in mammals. In addition, the regression of CL is necessary for the initiation of the estrous cycle. Extensive research has shown that the prostaglandin F2α (PGF2α) induces the regression of CL in ruminants. However, the mechanisms of endoplasmic reticulum (ER) stress and autophagy in the regression of goat CL induced by PGF2α are still unclear. In this study, ovaries of dioestrus goats and goats that were 3 months pregnant were collected to detect the location of the ER stress-related protein GRP78. The relationship between the different stages of the luteal phase of goat CL during the estrous cycle and changes in the expression of ER stress-related proteins and autophagy-related proteins was confirmed by western blot analysis. The results showed that both ER stress and autophagy were activated in the late luteal phase of the goat CL. To reveal the function of ER stress and autophagy in the CL regression process induced by PGF2α, we used 4-phenyl butyric acid (4-PBA) and chloroquine (CQ) for inhibiting ER stress and autophagy, respectively. Through the apoptotic rate detected by the flow cytometry and the expression of ER stress- and autophagy-related proteins detected by western blotting, we demonstrated that ER stress promoted goat luteal cell apoptosis and autophagy, and that apoptosis can be enhanced by the inhibition of autophagy. In addition, knockdown of EIF2S1, which blocked the PERK pathway activation, promoted apoptosis by reducing autophagy in goat luteal cells treated with PGF2α. In conclusion, our study indicates that ER stress promotes goat luteal cell apoptosis to regulate the regression of CL and activates autophagy to inhibit the goat luteal cell apoptosis via PERK signaling pathway.
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