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Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [ChIP-seq]

ABSTRACT: Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [ChIP-seq]

PROVIDER: PRJNA412202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11173408.fastq.gz	Fastqsanger.gz
	SRR11173409.fastq.gz	Fastqsanger.gz
	SRR11484901.fastq.gz	Fastqsanger.gz
	SRR11484902.fastq.gz	Fastqsanger.gz
	SRR11484903.fastq.gz	Fastqsanger.gz

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Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging

Project description:Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging

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Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [RNA-seq]

Project description:Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [RNA-seq]

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Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [ChIP-seq]

Project description:Mesenchymal stem/stromal cells (MSCs) are multipotent progenitor cells with multilineage differentiation potentials. We previously reported histone demethylases KDM4B promoted osteogenesis and inhibited adipogenesis of human MSCs. To identify genome-wide enrichments of KDM4B and the changes in H3K9me3 marks when loss of KDM4B, Primary MSCs were isolated from Prx1Cre; Kdm4bf/f mice and control mice. ChIP-seq assay was performed using KDM4B, H3K9me3 and H3 antibody, respectively.

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Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging

Project description:This SuperSeries is composed of the SubSeries listed below.

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Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [RNA-seq]

Project description:Primary mMSCs were cultured in control medium (Con), containing DMEM and 15% FBS, or were subjeucted to osteogenic induction (OI) for 2 days. RNA was isolated using RNeasy Mini Kit (Qiagen, Cat#74104) from three biological replicates of primary MSCs from Prx1Cre;Kdm4bf/f mice and control mice. Total RNA was then purified with Dynabeads™ mRNA Purification Kit (Invitrogen, Cat#61006). RNA-seq libraries were constructed using Stranded RNA-Seq Library Preparation Kit (Kapa Biosystems, Cat#KK8400), and sequenced using an illumina HiSeq 3000 sequencer at the Technology Center for Genomics & Bioinformatics (TCGB) core at UCLA.

2021-02-10 | GSE104258 | GEO

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Project description:chromatin immunoprecipitation sequencing (ChIP-seq) was performed to identify the targeted genes of kdm4b

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Expression analysis of blastocysts in Kdm4b-PEs

Project description:To identify the genes that are controled by H3K9me3 modification in PEs, we conducted transcriptome analysis using Egfp-, Kdm4b-PEs, and IVF embryos at blastocyst stages. Kdm4b or Egfp mRNA injected oocytes were parthenogenetically activated. IVF embryos were generated according to standard protcol. All embryos were cultured in KSOM medium for 120 hours after activation or sperm insemination. Five blastocysts per one biological replicate were pooled and analyzed.

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Project description:To investigate how histone demethylases KDM4B and KDM6B may be involved in osteogenic commitment of mesenchymal stem cells (MSCs), we performed gene expression profiling and comparison on control, KDM4B- and KDM6B-knockdown MSCs at different stages of osteogenic differentiation. Human MSCs infected with scramble shRNAs, shRNAs against KDM4B or KDM6B are treated with BMP4/7 for 0, 4 and 24hrs. Total RNA were extracted from these 9 samples.

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Histone demethylase KDM4B promotes DNA damage by activating long interspersed nuclear element-1

Project description:We assess whole-genome H3K9me3 distribution in cancer cells and find that H3K9me3 is largely enriched in long interspersed nuclear element-1 (LINE-1). A significant proportion of KDM4B-dependent H3K9me3 was located in evolutionarily young LINE-1 elements, which likely retain retrotransposition activity. Ectopic expression of KDM4B promoted LINE-1 expression, while depletion of KDM4B reduced it. Furthermore, KDM4B overexpression enhanced LINE-1 retrotransposition efficacy, copy number, and associated DNA damage, presumably via the histone demethylase activity of KDM4B. Breast cancer cell lines expressing high levels of KDM4B also exhibited increased LINE-1 expression and copy number compared with other cell lines. Pharmacological inhibition of KDM4B significantly reduced LINE-1 expression and DNA damage in breast cancer cells with excessive KDM4B. Our study not only identifies KDM4B as a novel regulator of LINE-1, but it also suggests an unexpected oncogenic role for KDM4B overexpression in tumorigenesis, providing clues for the development of new cancer prevention strategies and therapies.

2018-10-24 | GSE121642 | GEO

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