Doxorubicin-induced apoptosis in germinal vesicle (GV) oocytes☆

Bar‐Joseph, Hadas; Ben‐Aharon, Irit; Rizel, Shulamith; Stemmer, Salomon M.; Tzabari, Moran; Shalgi, Ruth

doi:10.1016/j.reprotox.2010.07.003

Cited by 85 publications

(63 citation statements)

References 54 publications

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“…As the role of these branches in autophagy induced by doxorubicin is still not clear (17)(18)(19), their contributions to autophagy induction by doxorubicin were examined. Doxorubicin enhanced expression of CHOP, a transcriptional regulator that is induced by all three arms of the UPR (Fig.…”

Section: Doxorubicin Decreases Er Stress-induced Autophagy Resulting mentioning

confidence: 99%

Autophagy Induced by Deficiency of Sphingosine-1-phosphate Phosphohydrolase 1 Is Switched to Apoptosis by Calpain-mediated Autophagy-related Gene 5 (Atg5) Cleavage

Lépine

Allegood

Edmonds

et al. 2011

Journal of Biological Chemistry

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Background:The switch between autophagy and apoptosis is an important and complicated process that is not well understood. Results: Doxorubicin treatment switches protective autophagy in sphingosine-1-phosphate phosphohydrolase-1 (SPP1)-depleted cells to apoptosis, increasing ceramide synthesis that enhances calpain activation and cleavage of pro-autophagic Atg5, generating a pro-apoptotic fragment. Conclusion: Depletion of SPP1 sensitizes cells to doxorubicin-induced apoptosis. Significance: Sphingolipid metabolites are involved in the cross-talk between autophagy and apoptosis.

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Section: Doxorubicin Decreases Er Stress-induced Autophagy Resulting mentioning

confidence: 99%

Autophagy Induced by Deficiency of Sphingosine-1-phosphate Phosphohydrolase 1 Is Switched to Apoptosis by Calpain-mediated Autophagy-related Gene 5 (Atg5) Cleavage

Lépine

Allegood

Edmonds

et al. 2011

Journal of Biological Chemistry

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“…WT and IL-1α-KO female mice at various ages were primed with gonadotropins as previously described (59). Ovulated cumulus-oocyte complexes were isolated from the oviductal ampullae into M2 medium (Sigma) 16-18 h after human chorionic gonadotropin administration.…”

Section: Methodsmentioning

confidence: 99%

Interleukin-1 deficiency prolongs ovarian lifespan in mice

Uri-Belapolsky

Shaish

Eliyahu

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Oocyte endowment dwindles away during prepubertal and adult life until menopause occurs, and apoptosis has been identified as a central mechanism responsible for oocyte elimination. A few recent reports suggest that uncontrolled inflammation may adversely affect ovarian reserve. We tested the possible role of the proinflammatory cytokine IL-1 in the age-related exhaustion of ovarian reserve using IL-1α and IL-1β-KO mice. IL-1α-KO mice showed a substantially higher pregnancy rate and litter size compared with WT mice at advanced age. The number of secondary and antral follicles was significantly higher in 2.5-mo-old IL-1α-KO ovaries compared with WT ovaries. Serum anti-Müllerian hormone, a putative marker of ovarian reserve, was markedly higher in IL-1α-KO mice from 2.5 mo onward, along with a greater ovarian response to gonadotropins. IL-1β-KO mice displayed a comparable but more subtle prolongation of ovarian lifespan compared with IL-1α-KO mice. The protein and mRNA of both IL-1α and IL-1β mice were localized within the developing follicles (oocytes and granulosa cells), and their ovarian mRNA levels increased with age. Molecular analysis revealed decreased apoptotic signaling [higher B-cell lymphoma 2 (BCL-2) and lower BCL-2-associated X protein levels], along with a marked attenuation in the expression of genes coding for the proinflammatory cytokines IL-1β, IL-6, and TNF-α in ovaries of IL-1α-KO mice compared with WT mice. Taken together, IL-1 emerges as an important participant in the age-related exhaustion of ovarian reserve in mice, possibly by enhancing the expression of inflammatory genes and promoting apoptotic pathways.

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“…Только высокодоз-ная ПХТ полностью истощает ткань яичника, при-водя к стерильности [20][21][22]. В таких случаях полу-чение яйцеклеток с применением методов ВРТ не рекомендовано из-за проведенных ранее курсов ПХТ [23][24][25]. Поэтому сохранить фертильность па-циентки в таких случаях стало возможным только с использованием метода криоконсервации ткани яичника до начала ПХТ.…”

Section: Discussionunclassified