2019
DOI: 10.1369/0022155419881127
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Beclin 1 Interacts With Active Caspase-3 and Bax in Oocytes From Atretic Follicles in the Rat Ovary

Abstract: Oocyte cell death is a normal process in the mammalian ovary during follicular growth. Recent reports have demonstrated the presence of pro-apoptotic and pro-autophagic proteins during oocyte elimination. The goal of this study was to identify the interactions between proteins involved in different types of programmed cell death in the same oocyte during follicular atresia. We evaluated the presence of Beclin 1 and its interaction with the pro-apoptotic proteins active caspase-3, Bax, and Bak by means of histo… Show more

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Cited by 19 publications
(13 citation statements)
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“…Similarly, in a recent report [108], it was demonstrated that Bcl-2, by inhibiting Beclin 1, could result in the release of pro-apoptotic proteins i.e., Bak and Bax to promote apoptosis via activation of effector caspase-3 in atretic follicles in rat ovaries. It was also speculated that this interaction between Beclin 1 and Bcl-2 (or perhaps other Bcl-2 family members) could impair the ability of Bcl-2 to inhibit the pro-apoptotic proteins i.e., Bax and Bak, which in turn, might trigger cell apoptosis [108]. Recently it was also shown that Se deficiency led to an increased mRNA and protein expression of Bcl-2 and inhibited autophagy and induced apoptosis in chicken cardiomyocytes by inhibiting Bax/Bcl-2 and caspases-mediated cleavage of Beclin 1 [111].…”
Section: Expression Of Gpx1 Gpx3 Gpx4 Selenof Bcl-2 and P21mentioning
confidence: 64%
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“…Similarly, in a recent report [108], it was demonstrated that Bcl-2, by inhibiting Beclin 1, could result in the release of pro-apoptotic proteins i.e., Bak and Bax to promote apoptosis via activation of effector caspase-3 in atretic follicles in rat ovaries. It was also speculated that this interaction between Beclin 1 and Bcl-2 (or perhaps other Bcl-2 family members) could impair the ability of Bcl-2 to inhibit the pro-apoptotic proteins i.e., Bax and Bak, which in turn, might trigger cell apoptosis [108]. Recently it was also shown that Se deficiency led to an increased mRNA and protein expression of Bcl-2 and inhibited autophagy and induced apoptosis in chicken cardiomyocytes by inhibiting Bax/Bcl-2 and caspases-mediated cleavage of Beclin 1 [111].…”
Section: Expression Of Gpx1 Gpx3 Gpx4 Selenof Bcl-2 and P21mentioning
confidence: 64%
“…It has been shown that Bcl-2 can inhibit the autophagy via its strong independent interaction with Beclin 1 in a highly regulated manner in yeast and mammalian cell lines [107]. Similarly, in a recent report [108], it was demonstrated that Bcl-2, by inhibiting Beclin 1, could result in the release of pro-apoptotic proteins i.e., Bak and Bax to promote apoptosis via activation of effector caspase-3 in atretic follicles in rat ovaries. It was also speculated that this interaction between Beclin 1 and Bcl-2 (or perhaps other Bcl-2 family members) could impair the ability of Bcl-2 to inhibit the pro-apoptotic proteins i.e., Bax and Bak, which in turn, might trigger cell apoptosis [108].…”
Section: Expression Of Gpx1 Gpx3 Gpx4 Selenof Bcl-2 and P21mentioning
confidence: 81%
See 1 more Smart Citation
“…It has been documented that this apoptotic pathway is responsible for the expression of Bcl‐2 family members, the loss of mitochondrial transmembrane potential (MMP) and the release of cytochrome c from mitochondria to the cytoplasm 34 . Triggering the cascade reaction of the caspase family and activating caspase‐3 and finally triggering apoptosis 35 . The Bcl‐2 protein family includes pro‐apoptotic and anti‐apoptotic members, such as Bax and Bcl‐2.…”
Section: Discussionmentioning
confidence: 99%
“…CHOP can trigger the intrinsic apoptotic pathway through the inhibition of BCL2, BCL-XL, and MCL-1 and the upregulation of BIM, which regulates BAX-BAK-mediated mitochondrial outer membrane permeabilization, leading to Cyto C release and the Caspase cascade ( Hu et al, 2018 ; Kim and Kim, 2018 ). Previous studies have identified that the expression of key regulators of oocyte apoptosis (Bax and Caspase 3) is increased in mouse oocyte apoptosis ( Escobar et al, 2019 ; Wang F. et al, 2020 ; Wang L. et al, 2020 ). Overexpression of Bax modulates the mitochondrial ΔΨ m and triggers Cyto C release and induces the activation of Caspase 3, leading to DNA fragmentation and thereby oocyte apoptosis ( Chaube et al, 2014 ).…”
Section: Discussionmentioning
confidence: 99%