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Plat safeguards aged mouse oocytes against programmed cell death through activating the Erk1/2 pathway

ABSTRACT: Plat safeguards aged mouse oocytes against programmed cell death through activating the Erk1/2 pathway

PROVIDER: PRJNA1183336 | ENA |

REPOSITORIES: ENA

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Plat safeguards aged mouse oocytes against programmed cell death through activating the Erk1/2 pathway

Project description:Female reproductive aging is characterized by the decline in oocytes quality and developmental potentials, but the underlying mechanisms remain insufficiently investigated. In this study, we analyze the transcriptomes of individual oocytes from young and aged mice, identifying a distinct group of aged oocytes, which display morphological abnormalities, such as fragmentation and darkened cytoplasm. These defective aged oocytes show a global shrink in gene expression, with yet a notable expression increase in mitochondrial RNA. Further gene expression analysis indicates that these defective oocytes exhibit typical features of programmed cell death (PCD), and functional assays demonstrate that those oocytes are specifically subject to both apoptosis and ferroptosis. Blocking the PCD pathways largely reverses the defective morphology. Interestingly, the expression of tissue-type plasminogen activator (tPA, or Plat) decreases with age, and even becomes undetectable in defective oocytes. Loss of Plat expression in oocytes downregulates Erk1/2 pathway activity, closely resembling the effects observed in Erk1/2 deficiency. Combining with tPA-interactome assay, it is suggested that Plat functions as an upstream regulator of Erk1/2 pathway activity, likely through Erk1/2 phosphorylation. Supplementing exogenous tPA in oocyte cultures reduces defect rate and therefore improves oocyte quality. Collectively, our findings highlight Plat as a pivotal factor in protecting aged mouse oocytes from PCD, with potential implications for developing better clinical strategies to enhance oocyte quality in aging females.

2025-09-13 | GSE281294 | GEO

Growth hormone supplementation reduces aneuploidy and improves the quality of oocytes by activating ERK1/2 pathway in aged mice

Project description:The decline in oocyte quality is a limiting factor of female fertility; however, strategies to maintain the oocyte quality of aged women are not available. In this study, we showed that growth hormone (GH) supplementation in vivo not only alleviated the decline in oocyte number caused by aging, but also improved the quality and developmental potential of aged oocytes. Strikingly, GH supplementation reduced aneuploidy in aged oocytes. Proteomic analysis indicated that the ERK1/2 pathway was involved in the reduction in aneuploidy rate of aged oocytes, as confirmed both in vivo and in vitro. In addition, JAK2 might be involved in the regulation of ERK1/2 by GH in aged oocytes. Collectively, our findings revealed that GH supplementation protects oocytes from aging-related aneuploidy and enhances the quality of aged oocytes, and could be used to improve the outcome of assisted reproduction in aged women.

2023-07-20 | PXD039147 | Pride

BDNF secreted by mesenchymal stem cells improves the quality and development potential of aged oocytes by activating the ERK1/2 signaling pathway

Project description:Decreased oocyte quality is a major determinant of age-associated fertility decline which lacks an effective treatment strategy. The secretome of mesenchymal stem cells (MSC-sec) contains various bioactive factors and has the potential to improve oocyte quality. In this study, MSC-sec treatment significantly increased first polar body emission, improved spindle assembly, reduced aneuploidy rate, and promoted maternal mRNA degradation in aged mouse oocytes, whereas the addition of BDNF antibody blocked the effects of MSC-sec. Furthermore, BDNF treatment alone also improved the oocyte quality from aged mice. Mechanistically, both MSC-sec and BDNF activated the ERK1/2 signaling pathway to increase the expression of DAZL and BTG4 in aged oocytes. Furthermore, injection of MSC-sec or BDNF into aged mouse ovaries significantly improved oocyte quality and early embryonic development. Finally, we demonstrated that BDNF treatment increased both the fertilization rate and blastocyst formation of aged human oocytes. Our study identified BDNF as the functional component of MSC-sec to improve the quality and development potential of aged oocytes by activating the ERK1/2 signaling pathway, suggesting that BDNF has the potential to mitigate age-related decline in oocyte quality.

2025-04-02 | GSE263864 | GEO

Preventing CpG hypermethylation in oocytes safeguards mouse development

Project description:Preventing CpG hypermethylation in oocytes safeguards mouse development

| PRJNA983810 | ENA

Preventing CpG hypermethylation in oocytes safeguards mouse development [WGBS GVO]

Project description:Preventing CpG hypermethylation in oocytes safeguards mouse development [WGBS GVO]

| PRJNA983818 | ENA

Preventing CpG hypermethylation in oocytes safeguards mouse development [Cut&Run]

Project description:Preventing CpG hypermethylation in oocytes safeguards mouse development [Cut&Run]

| PRJNA983817 | ENA

Preventing CpG hypermethylation in oocytes safeguards mouse development [RNA-seq]

Project description:Preventing CpG hypermethylation in oocytes safeguards mouse development [RNA-seq]

| PRJNA983814 | ENA

Preventing CpG hypermethylation in oocytes safeguards mouse development [WGBS 4-cell]

Project description:Preventing CpG hypermethylation in oocytes safeguards mouse development [WGBS 4-cell]

| PRJNA1301835 | ENA

Preventing CpG hypermethylation in oocytes safeguards mouse development

Project description:Except for regulatory CpG-island sequences, genomes of most mammalian cells are widely DNA-methylated. In oocytes though, DNAme is largely confined to transcribed regions. The mechanisms restricting de novo DNAme in oocytes and the relevance thereof for zygotic genome activation and embryonic development are largely unknown. Here we show that KDM2A and KDM2B, two histone demethylases, prevent genome-wide accumulation of histone H3 lysine 36 di-methylation, thereby impeding DNMT3A-catalyzed DNAme. We demonstrate that aberrant DNAme at CpG-islands inherited from Kdm2a/Kdm2b double mutant oocytes represses gene transcription in two-cell embryos. Aberrant maternal DNAme impairs pre-implantation embryonic development which is suppressed by Dnmt3a deficiency during oogenesis. Hence, KDM2A/KDM2B are essential for confining the oocyte methylome, thereby conferring competence for early embryonic development. Our research implies that the reprogramming capacity eminent to early embryos is insufficient for erasing aberrant DNAme from maternal chromatin, and that early development is vulnerable to gene dosage haplo-insufficiency effects.

2025-03-27 | GSE234968 | GEO

BDNF secreted by mesenchymal stem cells improves the quality and development potential of aged oocytes by activating the ERK1/2 signaling pathway

Project description:BDNF secreted by mesenchymal stem cells improves the quality and development potential of aged oocytes by activating the ERK1/2 signaling pathway

| PRJNA1099639 | ENA

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