Lin Xin, Liu Xingting, Ma Yanfen, Mi Yuling, Zeng Weidong, Li Jian, Zhang Caiqiao
Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou, Zhejiang Province 310058, China.
Aging (Albany NY). 2018 Apr 29;10(4):819-832. doi: 10.18632/aging.101436.
After ovulation in mammals, rupture of mature follicles is reorganized into the corpus luteum that secrets progesterone (P) to stimulate endometrial development. The situation in birds differs considerably. Beyond ovulation the ruptured avian follicle forms a postovulatory follicle (POF) that is not considered analogous to mammalian corpus luteum. The function and regression mechanisms of avian POFs remain poorly understood. Here we investigated the changes in apoptotic and autophagic activities that were involved during POF degradation. Results showed that the structure and secretory function of POF3 manifested the most apparent deterioration during whole processes of regression. A TUENL assay revealed that the granulosa layer maintained longer viability than the theca layer. Importantly, mitochondrial apoptosis and endoplasmic reticulum (ER) stress-associated genes and proteins reached their highest levels in the granulosa cells of POF3. Beclin1 was distributed mainly in theca cells and coupled with LC3β-II accumulation, Sequestosome-1 (p62) degradation and Beclin1 elevation confirmed that autophagic activity had increased dramatically in the theca layer of POFs. These results indicate that the apoptosis of the granulosa cells from POFs occurs by mitochondrial apoptosis and ER stress and that a coherence of Beclin1-induced autophagy and caspase-induced apoptosis results in regression of theca layers of avian POFs.
在哺乳动物排卵后，成熟卵泡的破裂会重新组织形成黄体，黄体分泌孕酮（P）以刺激子宫内膜发育。鸟类的情况则有很大不同。排卵后，破裂的鸟类卵泡会形成排卵后卵泡（POF），一般认为它与哺乳动物的黄体并不类似。鸟类POF的功能和退化机制仍知之甚少。在此，我们研究了POF退化过程中凋亡和自噬活动的变化。结果显示，在整个退化过程中，POF3的结构和分泌功能表现出最明显的恶化。TUNEL检测显示，颗粒层比卵泡膜层维持更长时间的活力。重要的是，线粒体凋亡和内质网（ER）应激相关基因及蛋白在POF3的颗粒细胞中达到最高水平。Beclin1主要分布在卵泡膜细胞中，并且伴随着LC3β-II的积累，聚集体蛋白1（p62）的降解以及Beclin1的升高证实POF卵泡膜层的自噬活性显著增加。这些结果表明，POF颗粒细胞的凋亡通过线粒体凋亡和内质网应激发生，并且Beclin1诱导的自噬与半胱天冬酶诱导的凋亡协同作用导致鸟类POF卵泡膜层的退化。
