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KDM4B epigenetically protects against obesity and metabolic dysfunction [ChIP-seq]

ABSTRACT: Preadiocyte of Kdm4b KO mice was infected with control or Flag-KDM4B retrovirus and were differentiated to adipocyte. The well-differentiated adipocytes were harvested for ChIP-Seq with Flag antibody.

ORGANISM(S): Mus musculus

PROVIDER: GSE102148 | GEO | 2019/05/22

REPOSITORIES: GEO

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KDM4B epigenetically protects against obesity and metabolic dysfunction [gene expression]

Project description:KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Mechanistically, we determined that KDM4B directly controls the expression of multiple metabolic genes.

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KDM4B epigenetically protects against obesity and metabolic dysfunction

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KDM4B epigenetically protects against obesity and metabolic dysfunction

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

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KDM4B protects against obesity and metabolic dysfunction.

Project description:Although significant progress has been made in understanding epigenetic regulation of in vitro adipogenesis, the physiological functions of epigenetic regulators in metabolism and their roles in obesity remain largely elusive. Here, we report that KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis, and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Obesity in KDM4B-deficient mice was accompanied by hyperlipidemia, insulin resistance, and pathological changes in the liver and pancreas. Adipocyte-specific deletion of Kdm4b revealed that the adipose tissues were the main sites for KDM4B antiobesity effects. KDM4B directly controlled the expression of multiple metabolic genes, including Ppargc1a and Ppara Collectively, our studies identify KDM4B as an essential epigenetic factor for the regulation of metabolic health and maintaining normal body weight in mice. KDM4B may provide a therapeutic target for treatment of obesity.

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ChIP-seq of Danio rerio wild type and kdm4b mutant embryos to investigate kdm4b signaling

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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Transcriptomic analysis of KDM4B-mediated genes in AGS cells

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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.

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Transcriptomic analysis of KDM4B-mediated gene in C4-2B prostate cancer cells

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