Programmed cell senescence in skeleton during late puberty

Changjun Li, Yu Chai, Lei Wang, Bo Gao, Hao Chen, Peisong Gao, Feng-Quan Zhou, Xianghang Luo, Janet L. Crane, Bin Yu (), Xu Cao and Mei Wan ()
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Changjun Li: Johns Hopkins University School of Medicine
Yu Chai: Johns Hopkins University School of Medicine
Lei Wang: Johns Hopkins University School of Medicine
Bo Gao: Johns Hopkins University School of Medicine
Hao Chen: Johns Hopkins University School of Medicine
Peisong Gao: Johns Hopkins University School of Medicine
Feng-Quan Zhou: Johns Hopkins University School of Medicine
Xianghang Luo: The Xiangya Hospital of Central South University
Janet L. Crane: Johns Hopkins University School of Medicine
Bin Yu: Southern Medical University
Xu Cao: Johns Hopkins University School of Medicine
Mei Wan: Johns Hopkins University School of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Mesenchymal stem/progenitor cells (MSPCs) undergo rapid self-renewal and differentiation, contributing to fast skeletal growth during childhood and puberty. It remains unclear whether these cells change their properties during late puberty to young adulthood, when bone growth and accrual decelerate. Here we show that MSPCs in primary spongiosa of long bone in mice at late puberty undergo normal programmed senescence, characterized by loss of nestin expression. MSPC senescence is epigenetically controlled by the polycomb histone methyltransferase enhancer of zeste homolog 2 (Ezh2) and its trimethylation of histone H3 on Lysine 27 (H3K27me3) mark. Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and deletion of Ezh2 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired osteogenesis as well as osteoporosis in later life. Our data reveals a programmed cell fate change in postnatal skeleton and unravels a regulatory mechanism underlying this phenomenon.

Date: 2017
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DOI: 10.1038/s41467-017-01509-0

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