Histone demethylase Jmjd3 regulates osteoblast apoptosis through targeting anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bim

Biochimica Et Biophysica Acta
Di YangTatsuji Haneji

Abstract

Posttranslational modifications including histone methylation regulate gene transcription through directly affecting the structure of chromatin. Trimethylation of histone H3K27 (H3K27me3) contributes to gene silencing and the histone demethylase Jumonji domain-containing 3 (Jmjd3) specifically removes the methylation of H3K27me3, followed by the activation of gene expression. In the present study, we explored the roles of Jmjd3 in regulating osteoblast apoptosis. Knockdown of Jmjd3 promoted osteoblast apoptosis induced by serum deprivation with decreased mitochondrial membrane potential and increased levels of caspase-3 activation, PARP cleavage, and DNA fragmentation. B cell lymphoma-2 (Bcl-2), an anti-apoptotic protein, was down-regulated by knockdown of Jmjd3 through retaining H3K27me3 on its promoter region. Knockdown of Jmjd3 increased the pro-apoptotic activity of Bim through inhibiting ERK-dependent phosphorylation of Bim. Protein kinase D1 (PKD1), which stimulates ERK phosphorylation, decreased in the Jmjd3-knockdown cells and introduction of PKD1 relieved osteoblast apoptosis in the Jmjd3-knockdown cells through increasing ERK-regulated Bim phosphorylation. These results suggest that Jmjd3 regulates osteoblast apoptosi...Continue Reading

References

Jun 11, 2005·Cell Death and Differentiation·R LeyS J Cook
Jun 5, 2007·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Robert L JilkaStavros C Manolagas
Dec 8, 2007·Journal of Cellular Physiology·B EspinaP A Hulley
Feb 7, 2008·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Min LiangPhilippa A Hulley
May 13, 2010·Heredity·E R Gibney, C M Nolan
Jul 8, 2011·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Tetsuro YasuiSakae Tanaka
Jan 19, 2012·Cell Biochemistry and Function·Nando Dulal DasYoung Gyu Chai
Jul 12, 2012·Development·Conchi EstarásMarian A Martínez-Balbás
Jul 12, 2013·International Journal of Endocrinology·Ling-Juan LiuDing-An Mao
Aug 24, 2013·Endocrinology·Jeffery J FordJohn C Lee
Oct 10, 2013·The Journal of Biological Chemistry·Di YangTatsuji Haneji
Dec 20, 2013·Clinical Chemistry and Laboratory Medicine : CCLM·Peter VrtačnikBarbara Ostanek
Jun 14, 2014·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·Antero SalminenAnu Kauppinen
Aug 19, 2014·Nature·Panagiotis NtziachristosIannis Aifantis
Jan 15, 2015·Journal of Molecular Cell Biology·Feng ZhangCharlie Degui Chen
Apr 29, 2015·Journal of Cellular Biochemistry·Di YangTatsuji Haneji

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Citations

Mar 10, 2016·Biochimica Et Biophysica Acta·Patrick M PerrigueJan Barciszewski
Dec 18, 2016·Anatomical Science International·Tatsuji Haneji
Jan 31, 2017·Toxicological Research·Kyoung Ah Kang, Jin Won Hyun
Oct 14, 2017·Biological Trace Element Research·Feibo XuYanfei Li
Mar 1, 2017·Journal of Clinical Medicine·Di YangLihong Qiu
May 9, 2019·Journal of Molecular Cell Biology·Qi WangXiaoren Zhang
Mar 14, 2021·European Journal of Medicinal Chemistry·Marzieh SohrabiMohammad Mahdavi

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