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

GSE276769 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 6 samples Submitted 2024/11/06 Platform GPL24247
Summary
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.
Published in
Prenatal dexamethasone exposure reduces osteoprogenitor proliferation in mice via histone modifications at the Mkp-1 gene locus
Xie Y, Su J, Yang M et al. · Communications biology 2024 · PMID 39609620 · doi:10.1038/s42003-024-07288-x
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Also filed as BioProject PRJNA1158832 and SRA study SRP531664. Searching any of these in the dataset finder brings you back here.

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