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Non-cell Autonomous Mechanisms Control Mitochondrial Gene Dysregulation in Polycystic Ovary Syndrome

ABSTRACT: Non-cell Autonomous Mechanisms Control Mitochondrial Gene Dysregulation in Polycystic Ovary Syndrome

PROVIDER: PRJNA780022 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16936975_1.fastq.gz	Fastqsanger.gz
	SRR16936975_2.fastq.gz	Fastqsanger.gz
	SRR16936976_1.fastq.gz	Fastqsanger.gz
	SRR16936976_2.fastq.gz	Fastqsanger.gz
	SRR16936977_1.fastq.gz	Fastqsanger.gz

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Non-cell autonomous mechanisms control mitochondrial gene dysregulation in polycystic ovary syndrome.

Project description:Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with insulin resistance and impaired energy metabolism in skeletal muscle, the aetiology of which is currently unclear. Here, we mapped the gene expression profile of skeletal muscle from women with PCOS and determined if cultured primary myotubes retain the gene expression signature of PCOS in vivo. Transcriptomic analysis of vastus lateralis biopsies collected from PCOS women showed lower expression of genes associated with mitochondrial function, while the expression of genes associated with the extracellular matrix was higher compared to controls. Altered skeletal muscle mRNA expression of mitochondrial-associated genes in PCOS was associated with lower protein expression of mitochondrial complex II-V, but not complex I, with no difference in mitochondrial DNA content. Transcriptomic analysis of primary myotube cultures established from biopsies did not display any differentially expressed genes between controls and PCOS. Comparison of gene expression profiles in skeletal muscle biopsies and primary myotube cultures showed lower expression of mitochondrial and energy metabolism-related genes in vitro, irrespective of the group. Together, our results show that the altered mitochondrial-associated gene expression in skeletal muscle in PCOS is not preserved in cultured myotubes, indicating that the in vivo extracellular milieu, rather than genetic or epigenetic factors, may drive this alteration. Dysregulation of mitochondrial-associated genes in skeletal muscle by extracellular factors may contribute to the impaired energy metabolism associated with PCOS.

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Non-cell Autonomous Mechanisms Control Mitochondrial Gene Dysregulation in Polycystic Ovary Syndrome

Project description:The aim of this study was to gain further insight into the mechanisms leading to metabolic dysfunction in skeletal muscle in PCOS, and to determine whether primary myotubes retain the gene expression signature of PCOS in vivo. We investigated the transcriptomic profile of skeletal muscle tissue and primary myotube cultures from insulin resistant women with PCOS compared to healthy controls.

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Project description:Aberration in miRNA expression or DNA methylation is a causal factor for numerous pathological conditions including polycystic ovarian syndrome PCOS, a common endocrine disorders and leading cause of infertility. The epigenetic interactions between miRNA and DNA methylation remain unexplored in PCOS. Few studies have reported that the regulation of miRNAs in polycystic ovary syndrome(PCOS). Our study helps to understand the molecular pathogenesis of PCOS in human ovarian granulosa cells from the perspective of post-transcriptional level.

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Project description:Aberration in miRNA expression or DNA methylation is a causal factor for numerous pathological conditions including polycystic ovarian syndrome PCOS, a common endocrine disorders and leading cause of infertility. The epigenetic interactions between miRNA and DNA methylation remain unexplored in PCOS. Few studies have reported that the key genes and pathways involved in polycystic ovary syndrome(PCOS). Our study helps to understand the molecular pathogenesis of PCOS in human ovarian granulosa cells and identifiy genes and pathways that may be potential therapeutic targets for PCOS treatment..

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