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组蛋白H3K9去甲基化酶JMJD2B在脂肪生成过程中通过调节PPARγ和C/EBPα上的H3K9甲基化来激活脂肪生成。

Histone H3K9 Demethylase JMJD2B Activates Adipogenesis by Regulating H3K9 Methylation on PPARγ and C/EBPα during Adipogenesis.

作者信息

Jang Min-Kyung, Kim Ji-Hyun, Jung Myeong Ho

机构信息

School of Korean Medicine, Pusan National University, 49 Busandaehak-ro, Mulguem-eup, Yangsan-si, Gyeongnam, South Korea.

出版信息

PLoS One. 2017 Jan 6;12(1):e0168185. doi: 10.1371/journal.pone.0168185. eCollection 2017.

DOI:10.1371/journal.pone.0168185
PMID:28060835
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5218499/
Abstract

Previous studies have shown that tri- or di-methylation of histone H3 at lysine 9 (H3K9me3/me2) on the promoter of the peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα) contribute to the repression of PPARγ and C/EBPα and inhibition of adipogenesis in 3T3-L1 preadipocytes. The balance of histone methylation is regulated by histone methyltransferases and demethylases. However, it is poorly understood which demethylases are responsible for removing H3K9me3/me2 on the promoter of PPARγ and C/EBPα. JMJD2B is a H3K9me3/me2 demethylase that was previously shown to activate adipogenesis by promoting mitotic clonal expansion. Nevertheless, it remains unclear whether JMJD2B plays a role in the regulation of adipogenesis by removing H3K9me3/me2 on the promoter of PPARγ and C/EBPα and subsequently activating PPARγ and C/EBPα expression. Here, we showed that JMJD2B decreased H3K9me3/me2 on the promoter of PPARγ and C/EBPα, which in turn stimulated the expression of PPARγ and C/EBPα. JMJD2B knockdown using siRNA in 3T3-L1 preadipocytes repressed the expression of PPARγ and C/EBPα, resulting in inhibition of adipogenesis. This was accompanied by increased enrichment of H3K9me3/me2 on the promoter of PPARγ and C/EBPα. In contrast, overexpression of JMJD2B increased the expression of PPARγ and C/EBPα, which was accompanied by decreased enrichment of H3K9me3/me2 on the promoter and activated adipogenesis. Together, these results indicate that JMJD2B regulates PPARγ and C/EBPα during adipogenesis.

摘要

先前的研究表明，过氧化物酶体增殖物激活受体γ（PPARγ）和CCAAT/增强子结合蛋白α（C/EBPα）启动子上组蛋白H3赖氨酸9位点的三甲基化或二甲基化（H3K9me3/me2）有助于抑制PPARγ和C/EBPα，并抑制3T3-L1前脂肪细胞的脂肪生成。组蛋白甲基化的平衡由组蛋白甲基转移酶和去甲基酶调节。然而，对于哪些去甲基酶负责去除PPARγ和C/EBPα启动子上的H3K9me3/me2，人们了解甚少。JMJD2B是一种H3K9me3/me2去甲基酶，先前的研究表明它通过促进有丝分裂克隆扩增来激活脂肪生成。然而，JMJD2B是否通过去除PPARγ和C/EBPα启动子上的H3K9me3/me2，随后激活PPARγ和C/EBPα的表达，在脂肪生成的调节中发挥作用仍不清楚。在这里，我们表明JMJD2B降低了PPARγ和C/EBPα启动子上的H3K9me3/me2，这反过来又刺激了PPARγ和C/EBPα的表达。在3T3-L1前脂肪细胞中使用小干扰RNA（siRNA）敲低JMJD2B可抑制PPARγ和C/EBPα的表达，从而抑制脂肪生成。这伴随着PPARγ和C/EBPα启动子上H3K9me3/me2富集的增加。相反，JMJD2B的过表达增加了PPARγ和C/EBPα的表达，同时启动子上H3K9me3/me2的富集减少，并激活了脂肪生成。总之，这些结果表明JMJD2B在脂肪生成过程中调节PPARγ和C/EBPα。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/23652e326ae7/pone.0168185.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/05739e2e26c9/pone.0168185.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/38dfb57cac02/pone.0168185.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/4abce6d00aab/pone.0168185.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/188dfcf33f5b/pone.0168185.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/4f195b8b273c/pone.0168185.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/0b985fe8cfdd/pone.0168185.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/23652e326ae7/pone.0168185.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/05739e2e26c9/pone.0168185.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/38dfb57cac02/pone.0168185.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/4abce6d00aab/pone.0168185.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/188dfcf33f5b/pone.0168185.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/4f195b8b273c/pone.0168185.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/0b985fe8cfdd/pone.0168185.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60dd/5218499/23652e326ae7/pone.0168185.g007.jpg

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