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Programmed cell senescence in skeleton during late puberty

Author

Listed:
  • Changjun Li

    (Johns Hopkins University School of Medicine
    The Xiangya Hospital of Central South University)

  • Yu Chai

    (Johns Hopkins University School of Medicine
    Southern Medical University)

  • Lei Wang

    (Johns Hopkins University School of Medicine
    Southern Medical University)

  • 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
    Department of Pediatric Endocrinology, 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)

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.

Suggested Citation

  • Changjun Li & Yu Chai & Lei Wang & Bo Gao & Hao Chen & Peisong Gao & Feng-Quan Zhou & Xianghang Luo & Janet L. Crane & Bin Yu & Xu Cao & Mei Wan, 2017. "Programmed cell senescence in skeleton during late puberty," Nature Communications, Nature, vol. 8(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01509-0
    DOI: 10.1038/s41467-017-01509-0
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    Cited by:

    1. Yonggang Fan & Weixin Zhang & Xiusheng Huang & Mingzhe Fan & Chenhao Shi & Lantian Zhao & Guofu Pi & Huafeng Zhang & Shuangfei Ni, 2024. "Senescent-like macrophages mediate angiogenesis for endplate sclerosis via IL-10 secretion in male mice," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
    2. Yuyao Tian & Wuming Wang & Sofie Lautrup & Hui Zhao & Xiang Li & Patrick Wai Nok Law & Ngoc-Duy Dinh & Evandro Fei Fang & Hoi Hung Cheung & Wai-Yee Chan, 2022. "WRN promotes bone development and growth by unwinding SHOX-G-quadruplexes via its helicase activity in Werner Syndrome," Nature Communications, Nature, vol. 13(1), pages 1-20, December.

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