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Mutual regulation between GDF11 and TET2 prevents senescence in adipose tissue-derived mesenchymal stem cells

ABSTRACT: We implemented transcriptomic analyses of hADSCs treated with rGDF11 1, 2 and 6 days

ORGANISM(S): Homo sapiens

PROVIDER: GSE142761 | GEO | 2022/12/31

REPOSITORIES: GEO

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Mutual regulation between GDF11 and TET2 prevents senescence in adipose tissue-derived mesenchymal stem cells

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Project description:Human adipose derived stem cells (hADSCs) are an attractive multipotent stem cell source with therapeutic applicability in diverse fields for the repair and regeneration of acute and chronically damaged tissues.In the last few years there has been increased interest in hADSCs for tissue engineering applications; however, the molecular mechanisms especially the microRNAs underlying the regulation of hADSCs proliferation and differentiation are not fully understood. To this end, we profiled the global microRNA expression in hADSCs, fibroblasts and endothelial cells by using Exqion mercury LNATM (Exqion Inc) To identify the microRNAs significantly expressed in human adipose derived stem cells, eight samples were analyzed using Exqion mercury LNATM (Exqion Inc) including six hADSCs samples and human endothelial and fibroblast cells as controls.

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Project description:Human adipose derived stem cells (hADSCs) are an attractive multipotent stem cell source with therapeutic applicability in diverse fields for the repair and regeneration of acute and chronically damaged tissues. In the last few years there has been increased interest in hADSCs for tissue engineering applications; however, the molecular mechanisms underlying the regulation of hADSCs proliferation and differentiation are not fully understood. In an effort to reveal the functions essential for this process, we performed microarray (Agilent 4x44K Whole Human Genome Microarray Kit) to profile the global gene expression in the hADSCs by including human endothelial and fibroblast cells as controls. To identify the genes significantly expressed in human adipose derived stem cells, eight samples were analyzed using Agilent whole human genome microarray including six hADSCs samples and human endothelial and fibroblast cells as controls.

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Project description:Human adipose derived stem cells (hADSCs) are an attractive multipotent stem cell source with therapeutic applicability in diverse fields for the repair and regeneration of acute and chronically damaged tissues. In the last few years there has been increased interest in hADSCs for tissue engineering applications; however, the molecular mechanisms underlying the regulation of hADSCs proliferation and differentiation are not fully understood. In an effort to reveal the functions essential for this process, we performed microarray (Agilent 4x44K Whole Human Genome Microarray Kit) to profile the global gene expression in the hADSCs by including human endothelial and fibroblast cells as controls.

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Melatonin prevents senescence of canine adipose-derived mesenchymal stem cells through activating NRF2 and inhibiting ER stress.

Project description:Transplantation of adipose-derived mesenchymal stem cells (ADMSCs) can aid in the treatment of numerous diseases in animals. However, natural aging during in vitro expansion of ADMSCs prior to their use in transplantation restricts their beneficial effects. Melatonin is reported to exert biorhythm regulation, anti-oxidation, and anti-senescence effects in various animal and cell models. Herein, by using a senescent canine ADMSCs (cADMSCs) cell model subjected to multiple passages in vitro, we investigated the effects of melatonin on ADMSCs senescence. We found that melatonin alleviates endoplasmic reticulum stress (ERS) and cell senescence. MT1/MT2 melatonin receptor inhibitor, luzindole, diminished the mRNA expression levels and rhythm expression amplitude of Bmal1 and Nrf2 genes. Nrf2 knockdown blocked the stimulatory effects of melatonin on endoplasmic reticulum-associated degradation (ERAD)-related gene expression and its inhibitory effects on ERS-related gene expression. At the same time, the inhibitory effects of melatonin on the NF-?B signaling pathway and senescence-associated secretory phenotype (SASP) were blocked by Nrf2 knockdown in cADMSCs. Melatonin pretreatment improved the survival of cADMSCs and enhanced the beneficial effects of cADMSCs transplantation in canine acute liver injury. These results indicate that melatonin activates Nrf2 through the MT1/MT2 receptor pathway, stimulates ERAD, inhibits NF-?B and ERS, alleviates cADMSCs senescence, and improves the efficacy of transplanted cADMSCs.

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