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Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

ABSTRACT: Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

PROVIDER: PRJNA1158832 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30608224_1.fastq.gz	Fastqsanger.gz
	SRR30608224_2.fastq.gz	Fastqsanger.gz
	SRR30608225_1.fastq.gz	Fastqsanger.gz
	SRR30608225_2.fastq.gz	Fastqsanger.gz
	SRR30608226_1.fastq.gz	Fastqsanger.gz

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Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

Project description:Prenatal dexamethasone exposure (PDE) has long-term consequences in bone development. we investigated how PDE exerts persistent effect on bone metabolism in mouse offspring. Our results showed that PDE offspring exhibited reduced bone mass, fewer osteoblasts and diminished osteoprogenitors proliferation.And PDE increased MKP-1 expression, while decreasing H3 lysine 9 dimethylation (H3K9me2) at Mkp-1 gene locus. Mechanistically, dexamethasone suppressed osteoprogenitors proliferation by upregulating MKP-1 expression, notably through the inhibition of H3K9me2 modifications, which promoted demethylation and transcriptional activation of the Mkp-1 gene. Importantly, restoring histone methylation balance with PFI-90 treatment blocked the inhibitory effects of PDE on MAPK signaling in osteoprogenitors, and mitigated the detrimental impact of PDE on osteoprogenitor proliferation and bone development in the offspring. Therefore,we performed ChIP-seq for H3K9me2 to identify its role in related epigenetic changes.

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