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Related Experiment Videos

DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age.

Ha-Neui Kim1,2, Jianhui Chang3, Lijian Shao3

  • 1Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

Aging Cell
|April 13, 2017
PubMed
Summary

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This summary is machine-generated.

Aging bone loss stems from fewer bone-building cells and more bone breakdown. This study identifies age-related DNA damage and senescence in osteoprogenitors, driving bone loss. Senolytic drugs show promise in reversing these effects.

Area of Science:

  • Gerontology
  • Cell Biology
  • Bone Biology

Background:

  • Age-related bone loss involves reduced bone formation and increased resorption.
  • Osteoblast decline is linked to aging mesenchymal osteoblast progenitors, but their specific markers and causes are unknown.
  • Current research relies on in vitro cultures of mixed cell populations, limiting understanding of progenitor cell changes.

Purpose of the Study:

  • To identify specific markers for mesenchymal osteoblast progenitors.
  • To investigate age-dependent changes in osteoprogenitor cells.
  • To explore the role of senescence and DNA damage in age-related bone loss.

Main Methods:

  • Utilized Osx1-Cre;TdRFP mice to fluorescently label osteoprogenitors.
  • Quantified TdRFP-Osx1 cells in bone marrow from young (6 months) and old (24 months) mice.
Keywords:
ABT263GATA4NF-κBosteoblastsosteoporosisp21p53

Related Experiment Videos

  • Assessed markers of DNA damage, senescence (γH2AX, p53, p21CIP1), GATA4, NF-κB activation, and SASP gene expression.

    • Main Results:

    • Osteoprogenitor cell numbers (TdRFP-Osx1) decreased by over 50% in old mice.
    • Old osteoprogenitors showed DNA damage and senescence markers, including G1 arrest and increased p53/p21CIP1.
    • Old bone marrow stromal cells exhibited elevated SASP gene expression and supported increased osteoclast formation.
    • Senolytic drug ABT263 significantly attenuated these age-related changes.

    Conclusions:

    • Intrinsic defects, including DNA damage and senescence, in osteoprogenitor cells contribute to age-related bone loss.
    • These cellular changes lead to reduced osteoblast numbers and enhanced osteoclastogenesis.
    • Targeting senescent osteoprogenitors with senolytic drugs may offer a therapeutic strategy for age-related bone diseases.