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Transcriptome profiling identified dysregulated signaling related to adipogenesis, metabolism, and inflammation in polycystic ovary syndrome patients

ABSTRACT: Polycystic ovary syndrome (PCOS) is a female endocrine disorder characterized by hyperandrogenism, chronic anovulation, and polycystic ovaries. PCOS is often accompanied by symptoms such as insulin resistance, abdominal obesity, and chronic inflammation. Adipose tissue is a crucial endocrine organ involved in metabolic disorders. Metabolic issues and chronic inflammation in PCOS are linked to dysfunctional adipose tissue. Mesenchymal progenitor cells (MPCs) are the precursor cells of adipocytes and can regulate the immune system. In this study, we used induced pluripotent stem cells (iPSCs) from patients with PCOS to derive MPCs and compare the transcriptome profiles between PCOS and HC iPSC-derived MPCs. We also challenged iPSC-derived MPCs with testosterone to assess the impact of androgen on MPCs. We found that 1026 genes differed between PCOS and HC iPSC-derived MPCs. Gene set enrichment analysis showed adipogenesis and metabolic function were reduced, but the inflammatory response was raised in PCOS iPSC-derived MPCs. The critical signals for early adipogenesis, including TGFβ, BMP, WNT, and CEBPA, differed between PCOS and HC iPSC-derived MPCs. After adipogenic induction, mature adipocytes were lower in PCOS iPSC-derived MPCs than HC. Lipolysis, the process involved in fat metabolism, was lower in adipocytes derived from PCOS MPCs than in HC. The testosterone treatment results indicated that genes related to oxidative phosphorylation and fatty acid metabolism were upregulated in HC iPSC-derived MPCs but downregulated in PCOS iPSC-derived MPCs. Short-term androgen stimulation may benefit body functions in HC. The impact of testosterone varied among individuals with HC and PCOS, possibly because of a genetic tendency towards PCOS. This study explains important factors that help us understand PCOS.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267287 | GEO | 2024/08/16

REPOSITORIES: GEO

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Project description:The utility of human pluripotent stem cells as a tool for understanding disease and as a renewable source of cells for transplantation therapies is dependent on efficient differentiation protocols that convert these cells into relevant adult cell types. Here we report the robust and efficient differentiation of human pluripotent stem cells into adipocytes. We found that inducible expression of PPARG2 in pluripotent stem cell-derived mesenchymal progenitor cells programmed their development towards an adipocyte cell fate. Using this approach, multiple human pluripotent cell lines were differentiated into adipocytes with efficiencies of 85% to 90%. These pluripotent stem cell-derived adipocytes retained their identity independent of transgene expression, could be maintained in culture for several weeks, expressed mature markers, and exhibited mature functional properties such as lipid catabolism in response to a beta-adrenergic stimulus. Global transcriptional and lipid metabolomic analyses further confirmed the identity and maturity of these pluripotent stem cell-derived adipocytes. Mesenchymal progenitor cells (MPCs) derived from human embryonic stem cells hESCs and induced pluripotent stem cells (iPSCs) along with adipose-derived stromal vascular cells (ADSVCs) were subjected to induction of PPAR2 and compared to primary fat samples. Overall 2 ADSVC (ADSVC 24 nd 49) lines, 1 hESC (HUES9) line and 1 iPSC (BJRiPS) line were differentiated into MPCs, PPAR2 programmed, and compared to untreated MPCs and primary fat samples from 2 individuals. Each condition is either represented in duplicate or triplicate on affymetrix HuGene-1_0-st arrays. MPCs derived from the hESC lines HUES2 and HUES8, ADSVCs, and BJRiPS were also run on a separate platform (HG-U133_Plus_2) with more GEO presence to facilitate analysis (34 samples, two platforms total). Supplementary file(s): GeneSymbol-collapsed data represent the final normalized data used for analyses in the manuscript.

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Transcriptome profiling identified dysregulated signaling related to adipogenesis, metabolism, and inflammation in polycystic ovary syndrome patients

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