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Identification of Senescent Cells in the Bone Microenvironment
Joshua N Farr1, Daniel G Fraser1, Haitao Wang2
1Robert and Arlene Kogod Center on Aging and Endocrine Research Unit, Mayo Clinic College of Medicine, Rochester, MN, USA.
Summary
Cellular senescence, marked by p16Ink4a upregulation, increases in mouse bone cells with age. Senescent osteocytes and myeloid cells secrete factors contributing to age-related bone loss.
Area of Science:
- Gerontology and Cellular Biology
- Bone Biology and Aging
- Senescence and SASP
Background:
- Cellular senescence is a key aging mechanism, characterized by cell cycle arrest and altered secretomes (SASP).
- Senescent cells accumulate with age, contributing to degenerative diseases like osteoporosis.
- Identifying senescent cells in the bone microenvironment in vivo is crucial for understanding age-related bone pathologies.
Purpose of the Study:
- To investigate which bone cell types undergo senescence in vivo during aging.
- To analyze the senescence-associated secretory phenotype (SASP) in aged bone cells.
- To explore the potential role of senescent bone cells in age-related bone loss.
Main Methods:
- Analysis of senescence markers (p16Ink4a, SADS, TIFs) in highly enriched bone/marrow cell populations from young and old mice without in vitro culture.
- Quantification of SASP marker expression in isolated osteocytes and myeloid cells.
- Comparison of senescence and SASP markers between young (6 months) and old (24 months) mice.
Main Results:
- Aging significantly increased p16Ink4a expression in B cells, T cells, myeloid cells, osteoblast progenitors, osteoblasts, and osteocytes.
- Senescent osteocytes (SADS) were significantly more prevalent in old mice (11%) compared to young mice (2%).
- Osteocytes from old mice exhibited increased telomere dysfunction-induced foci (TIFs) and higher expression of SASP markers, with myeloid cells also showing age-associated SASP upregulation.
Conclusions:
- Cellular senescence affects multiple bone cell lineages with aging, with osteocytes and myeloid cells predominantly exhibiting the SASP.
- Accumulation of senescent osteocytes and their SASP may contribute to age-related bone loss.
- Targeting senescent cells in the bone microenvironment presents a potential therapeutic strategy for osteoporosis.
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