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Environmental dose of Bisphenol S exposure to brown adipose tissue accelerates aging

ABSTRACT: Environmental dose of Bisphenol S exposure to brown adipose tissue accelerates aging

PROVIDER: PRJNA1162646 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30717085_1.fastq.gz	Fastqsanger.gz
	SRR30717085_2.fastq.gz	Fastqsanger.gz
	SRR30717086_1.fastq.gz	Fastqsanger.gz
	SRR30717086_2.fastq.gz	Fastqsanger.gz
	SRR30717087_1.fastq.gz	Fastqsanger.gz

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Environmental dose of Bisphenol S exposure to brown adipose tissue accelerates aging

Project description:Bisphenol S (BPS), a common industrial chemical, is increasingly recognized for its potential to disrupt physiological functions even at environmental doses. In this study, we investigated the effects of BPS exposure on lifespan and health span using Caenorhabditis elegans and mouse models. We found that BPS accumulates in brown adipose tissue (BAT), inducing BAT aging by triggering mitochondrial dysfunction, chronic inflammation, altered intercellular communication, cellular senescence, deregulated nutrient-sensing pathways, impaired macroautophagy, and loss of proteostasis. These changes accelerated aging in multiple organs, including the heart, liver, kidneys, lungs, and skeletal muscle. Notably, BAT transplantation experiments revealed that BAT from BPS-exposed mice induced accelerated aging in non-exposed mice, while BAT from non-exposed mice mitigated aging in BPS-exposed mice. In summary, this study is the first to demonstrate that environmental doses of BPS promote systemic aging by disrupting BAT energy metabolism.

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Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development.

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Project description:Dexamethasone (DEX), a synthetic ligand for glucocorticoid receptor (GR), is routinely used to stimulate adipogenesis in culture. GR-depleted preadipocytes show adipogenesis defects one week after induction of differentiation. However, it has remained unclear whether GR is required for adipogenesis in vivo. By deleting GR in precursors of brown adipocytes, we found unexpectedly that GR is dispensable for brown adipose tissue development in mice. In culture, GR-deficient primary or immortalized white and brown preadipocytes showed severely delayed adipogenesis one week after induction of differentiation. However, when differentiation was extended to 3 weeks, GR-deficient preadipocytes showed similar levels of adipogenesis marker expression and lipid accumulation as the wild type cells, indicating that DEX-bound GR accelerates, but is dispensable for, adipogenesis. Consistently, DEX accelerates, but is dispensable for, adipogenesis in culture. We show that DEX-bound GR accelerates adipogenesis by directly promoting the expression of adipogenic transcription factors C/EBPb, C/EBPd, C/EBPa, KLF5, KLF9 and PPARg in the early phase of differentiation. Mechanistically, DEX-bound GR recruits histone H3K27 acetyltransferase CBP to promote activation of C/EBPb-primed enhancers of adipogenic genes. These results clarify the role of GR in adipogenesis in vivo and demonstrate that DEX-mediated activation of GR accelerates, but is dispensable for, adipogenesis.

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