2018
DOI: 10.18632/aging.101436
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Abstract: After ovulation in mammals, rupture of mature follicles is reorganized into the corpus luteum that secrets progesterone (P4) 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 inv… Show more

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Cited by 14 publications
(14 citation statements)
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“…Activated endoplasmic reticulum stress (ER-stress) and the mitochondrion apoptosis pathway are deleterious for GC survival [ 13 ]. Firstly, overactivation of ER-stress and activation of the mitochondrion apoptosis signaling pathway could trigger an intracellular calcium ion imbalance [ 14 ].…”
Section: Introductionmentioning
confidence: 99%
“…Activated endoplasmic reticulum stress (ER-stress) and the mitochondrion apoptosis pathway are deleterious for GC survival [ 13 ]. Firstly, overactivation of ER-stress and activation of the mitochondrion apoptosis signaling pathway could trigger an intracellular calcium ion imbalance [ 14 ].…”
Section: Introductionmentioning
confidence: 99%
“…A previous study reported that RAB11A may act as a major regulator of membrane delivery during cytokinesis (Chu et al, 2009) and plays a supporting role in autophagy (Huttenhower et al, 2009). The regression of the chicken postovulatory follicle is mediated by autophagy (Lin et al, 2018), and autophagy signaling pathways are critical in controlling broodiness in the goose (Yu et al, 2016). During the follicular growth process, most SYF follicles undergo atresia (Hocking, 2009), which involves a complex array of mechanisms that modulate GC and TC apoptosis (Johnson, 2003;Lebedev et al, 2006;Kim et al, 2016).…”
Section: Discussionmentioning
confidence: 99%
“…Imbalance of Ca 2+ concentration in the ER can also induce ER stress [10]. As markers of ER stress, calreticulin (CALR) and glucose-regulated protein 78 (GRP78) were upregulated when ER stress occurs [11,12]. CALR is the major calciumbinding molecular chaperone in ER and is responsible for controlling Ca 2+ release into cytoplasm to participate in the reactions of the misfolded proteins and regulate cell apoptosis [13].…”
Section: Introductionmentioning
confidence: 99%
“…TEM observation and IF staining demonstrated that ER stress appeared in whole follicles, whereas 13 Oxidative Medicine and Cellular Longevity ER stress mainly occurred in the GCs of follicles in D580 hens, accompanied with ER degenerative changes (swelling, hyperplasia, concentric circles, etc.) [12]. Subsequently, we examined the expression of GRP78 and CALR (ER stress markers), the key transcription factor ATF4 in the downstream of the UPR signaling pathway, and the ER stressmediated apoptotic transcription factors CHOP and caspase12 in the follicles.…”
mentioning
confidence: 99%