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• W2084440981 abstract "ObjectiveCigarette smoking is a lifestyle behavior associated with delayed conception, decreased success in assisted reproductive technologies and premature ovarian failure. However, the mechanisms underlying cigarette smoke (CS) induced depletion of the primordial follicle population is incompletely understood. We recently reported that CS exposure-induced follicle loss, decreased superoxide dismutase 2 expression (suggestive of mitochondrial loss/damage), and increased autophagolysosomes (indicative of autophagy pathway activation). We hypothesize that CS exposure disrupts mitochondrial repair mechanisms leading to the loss of follicles via autophagy-mediated granulosa cell (GC) death.DesignExperimental lab animal study.Materials and MethodsMice were exposed to CS or room air for 8 weeks. Ovaries were processed for histology, Western blotting and real time PCR. Treatment effects were tested using t-test and data expressed as mean±SEM. A P≤0.05 was considered significant.ResultsCS exposed mice had decreased expression of proteins involved in mitochondrial repair (pro-fusion proteins mitofusin 1 and 2) and increased expression of a pro-fission protein, Parkin, suggesting that CS exposure triggers mitochondrial damage. Using a gene array for autophagy-related genes, we found significant changes in the expression of genes involved in vacuole formation (Becn1, Gabarapl1, Map1lc3a/b), autophagy regulation (Bad, Bak1, CDKN1B, Sqstm1), protein ubiquitination (Atg7), and protein transport (Gabarap, Rab24). Real time PCR analysis was performed to validate results. In addition, Western blot analysis revealed that expression of Beclin 1 and LC3 (pro-autophagy) were significantly up-regulated, while Bcl-2 (autophagy inhibitor) was down-regulated following CS exposure representative of an average daily smoker.ConclusionOur data suggest that CS exposure induces dysfunction of mitochondrial repair mechanisms in GCs, leading to autophagy, a novel alternative cell death pathway resulting in follicle loss. ObjectiveCigarette smoking is a lifestyle behavior associated with delayed conception, decreased success in assisted reproductive technologies and premature ovarian failure. However, the mechanisms underlying cigarette smoke (CS) induced depletion of the primordial follicle population is incompletely understood. We recently reported that CS exposure-induced follicle loss, decreased superoxide dismutase 2 expression (suggestive of mitochondrial loss/damage), and increased autophagolysosomes (indicative of autophagy pathway activation). We hypothesize that CS exposure disrupts mitochondrial repair mechanisms leading to the loss of follicles via autophagy-mediated granulosa cell (GC) death. Cigarette smoking is a lifestyle behavior associated with delayed conception, decreased success in assisted reproductive technologies and premature ovarian failure. However, the mechanisms underlying cigarette smoke (CS) induced depletion of the primordial follicle population is incompletely understood. We recently reported that CS exposure-induced follicle loss, decreased superoxide dismutase 2 expression (suggestive of mitochondrial loss/damage), and increased autophagolysosomes (indicative of autophagy pathway activation). We hypothesize that CS exposure disrupts mitochondrial repair mechanisms leading to the loss of follicles via autophagy-mediated granulosa cell (GC) death. DesignExperimental lab animal study. Experimental lab animal study. Materials and MethodsMice were exposed to CS or room air for 8 weeks. Ovaries were processed for histology, Western blotting and real time PCR. Treatment effects were tested using t-test and data expressed as mean±SEM. A P≤0.05 was considered significant. Mice were exposed to CS or room air for 8 weeks. Ovaries were processed for histology, Western blotting and real time PCR. Treatment effects were tested using t-test and data expressed as mean±SEM. A P≤0.05 was considered significant. ResultsCS exposed mice had decreased expression of proteins involved in mitochondrial repair (pro-fusion proteins mitofusin 1 and 2) and increased expression of a pro-fission protein, Parkin, suggesting that CS exposure triggers mitochondrial damage. Using a gene array for autophagy-related genes, we found significant changes in the expression of genes involved in vacuole formation (Becn1, Gabarapl1, Map1lc3a/b), autophagy regulation (Bad, Bak1, CDKN1B, Sqstm1), protein ubiquitination (Atg7), and protein transport (Gabarap, Rab24). Real time PCR analysis was performed to validate results. In addition, Western blot analysis revealed that expression of Beclin 1 and LC3 (pro-autophagy) were significantly up-regulated, while Bcl-2 (autophagy inhibitor) was down-regulated following CS exposure representative of an average daily smoker. CS exposed mice had decreased expression of proteins involved in mitochondrial repair (pro-fusion proteins mitofusin 1 and 2) and increased expression of a pro-fission protein, Parkin, suggesting that CS exposure triggers mitochondrial damage. Using a gene array for autophagy-related genes, we found significant changes in the expression of genes involved in vacuole formation (Becn1, Gabarapl1, Map1lc3a/b), autophagy regulation (Bad, Bak1, CDKN1B, Sqstm1), protein ubiquitination (Atg7), and protein transport (Gabarap, Rab24). Real time PCR analysis was performed to validate results. In addition, Western blot analysis revealed that expression of Beclin 1 and LC3 (pro-autophagy) were significantly up-regulated, while Bcl-2 (autophagy inhibitor) was down-regulated following CS exposure representative of an average daily smoker. ConclusionOur data suggest that CS exposure induces dysfunction of mitochondrial repair mechanisms in GCs, leading to autophagy, a novel alternative cell death pathway resulting in follicle loss. Our data suggest that CS exposure induces dysfunction of mitochondrial repair mechanisms in GCs, leading to autophagy, a novel alternative cell death pathway resulting in follicle loss." @default.
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• W2084440981 title "Dysregulation of mitochondrial dynamics and activation of the autophagy cascade occur in a mouse model of cigarette smoke-induced ovarian follicle loss" @default.
• W2084440981 doi "https://doi.org/10.1016/j.fertnstert.2012.07.805" @default.
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