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H3K27me3 modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury [CUT&Tag]

ABSTRACT: H3K27me3 modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury [CUT&Tag]

PROVIDER: PRJNA989644 | ENA |

REPOSITORIES: ENA

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H3K27me3 modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury [CUT&Tag]

Project description:Chemotherapy-induced ovarian damage and infertility are significant concerns for women of childbearing age with cancer, but the underlying mechanisms are still not fully understood. Our study revealed a close association between H3K27me3 and cyclophosphamide (CTX)-induced ovarian damage, especially in granulosa cells.

2023-11-22 | GSE236296 | GEO

H3K27me3 modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury

Project description:H3K27me3 modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury

| PRJNA988016 | ENA

H3K27me3 modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury

Project description:Chemotherapy-induced ovarian damage and infertility are significant concerns for women of childbearing age with cancer, but the underlying mechanisms are still not fully understood. Our study revealed a close association between the loss of H3K27me3 and cyclophosphamide (CTX)-induced ovarian damage.

2023-11-22 | GSE235907 | GEO

The EZH2-H3K27me3 axis modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury.

Project description:Chemotherapy-induced ovarian damage and infertility are significant concerns for women of childbearing age with cancer; however, the underlying mechanisms are still not fully understood. Our study has revealed a close association between epigenetic regulation and cyclophosphamide (CTX)-induced ovarian damage. Specifically, CTX and its active metabolite 4-hydroperoxy cyclophosphamide (4-HC) were found to increase the apoptosis of granulosa cells (GCs) by reducing EZH2 and H3K27me3 levels, both in vivo and in vitro. Furthermore, RNA-seq and CUT&Tag analyses revealed that the loss of H3K27me3 peaks on promoters led to the overactivation of genes associated with transcriptional regulation and apoptosis, indicating that stable H3K27me3 status could help to provide a safeguard against CTX-induced ovarian damage. Administration of the H3K27me3-demethylase inhibitor, GSK-J4, prior to CTX treatment could partially mitigate GC apoptosis by reversing the reduction of H3K27me3 and the aberrant upregulation of specific genes involved in transcriptional regulation and apoptosis. GSK-J4 could thus potentially be a protective agent for female fertility when undergoing chemotherapy. The results provide new insights into the mechanisms for chemotherapy injury and future clinical interventions for fertility preservation.

| S-EPMC10646043 | biostudies-literature

Androgens Regulate Ovarian Gene Expression through Modulation of H3K27me3 in Granulosa Cells [RNA-Seq]

Project description:This study reports androgen-induced gene expression in granulosa cells of the ovary and provides a molecular insight of how androgens regulate granulosa cell gene expression through modulating the epigenetic mark H3K27me3.

2020-06-19 | GSE152727 | GEO

Androgens Regulate Ovarian Gene Expression through Modulation of H3K27me3 in Granulosa Cells [ChIP-seq]

2020-06-19 | GSE152791 | GEO

HO-1 modulates ferroptosis via ROS-mediated mitochondrial dysfunction in cyclophosphamide -induced ovarian granulosa cells

Project description:Abnormal granulosa cells (GCs) death contributes to cyclophosphamide (CTX) -induced primary ovarian insufficiency (POI). To investigate the contribution of GCs in POI, gene profiles of GCs exposed to CTX were assessed using RNA-Seq and bioinformatics analysis. The results showed the differentially expressed genes (DEGs) are enriched in ferroptosis-related pathway, which is correlated with the upregulated Heme oxygenase 1 (HO-1) and downregulated glutathione peroxidase-4 (GPX4). Using CTX-induced cell culture (COV434 and KGN cells), the levels of iron, reactive oxygen species (ROS), lipid peroxide, mitochondrial superoxide, mitochondrial morphology and mitochondrial membrane potential (MMP) were detected by DCFDA, MitoSOX, C11-BODIPY, MitoTracker, Nonylacridine Orange (NAO), JC-1 and transmission electron microscopy respectively. The results showed that iron overload and disrupting ROS, including cytoROS, mtROS and lipROS homeostasis by HO-1 upregultion could induce ferroptosis via mitochondrial dysfunction in CTX-induced GCs. Moreover, HO-1 inhibition could suppress ferroptosis induced GPX4 depletion. This implies the role of ROS in CTX-induced ferroptosis and highlighted the effect of HO-1 modulators of improving CTX-induced ovarian damage, which may provide a theoretical basis for preventing or restoring GC and ovarian function in patients with POI.

2023-10-30 | GSE243720 | GEO

MIR143 Inhibits Steroidogenesis and Induces Apoptosis Repressed by H3K27me3 in Granulosa Cells.

Project description:The granulosa cell growth factor and apoptotic factor are two factors to determine follicular apoptosis. Whether ssc-miR-143-3p (MIR143) plays as an apoptosis factor in porcine granulosa cells (pGCs) remain unclear. This study tries to investigate what function of MIR143 is and how MIR143 gets these functions in pGCs from 3 to 5 mm medium-sized follicles. Firstly, 5' RACE was used to identify the structure of MIR143, and in situ hybridization, qPCR, and DNA pull-down were employed to exhibit the spatio-temporal expression and transcriptional regulation of MIR143. Furthermore, ELISA, Western blotting, and flow cytometry were adopted to explore the functions of MIR143 in pGCs. It was found that MIR143 was an exonic miRNA located in host gene LOC100514340 with an increasing expression during follicular growth. Moreover, MIR143 suppressed steroidogenesis related genes of HSD17?4, ER1, and PTGS2, negatively regulating estrogen, androgen, progesterone, and prostaglandin. MIR143 induced the apoptosis via activation of BAX-dependent Caspase 3 signaling. Furthermore, H3K27me3 influenced the recruitment of transcription factors and binding proteins to repress MIR143 transcription. At last, H3K27me3 agonist with MIR143 inhibition activated steroidogenesis but repressed apoptosis. These findings suggest that H3K27me3-mediated MIR143 inhibition play a critical role in follicular atresia by regulating cell apoptosis and steroidogenesis, which will provide useful information for further investigations of H3K27me3-miediated MIR143 epigenetic regulation in follicular growth in mammals.

| S-EPMC7604341 | biostudies-literature

HO-1 modulates ferroptosis via ROS-mediated mitochondrial dysfunction in cyclophosphamide -induced ovarian granulosa cells

Project description:HO-1 modulates ferroptosis via ROS-mediated mitochondrial dysfunction in cyclophosphamide -induced ovarian granulosa cells

| PRJNA1019699 | ENA

Androgens Regulate Ovarian Gene Expression through Modulation of H3K27me3 in Granulosa Cells

Project description:Androgens Regulate Ovarian Gene Expression through Modulation of H3K27me3 in Granulosa Cells

| PRJNA640403 | ENA