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Transit-amplifying cell frequency and cell cycle kinetics are altered in aged epidermis
Alexandra Charruyer1, Chantal O Barland, Lili Yue
1Department of Dermatology, University of California, San Francisco, California 94121, USA.
The Journal of Investigative Dermatology
|May 22, 2009
Summary
Aging epidermis shows slower wound healing due to increased transit-amplifying (TA) cells, not stem cells. Aged TA cells persist longer, but individual aged stem and TA cells have reduced proliferative capacity, suggesting a compensatory mechanism.
Area of Science:
- Dermatology
- Cell Biology
- Aging Research
Background:
- Epidermal proliferation decreases with age, leading to slower wound healing.
- Previous studies suggested altered epidermal stem cell (EpiSC) frequency in aged skin.
- The specific contributions of stem and transit-amplifying (TA) cell compartments to age-related proliferation changes were unclear.
Purpose of the Study:
- To investigate quantitative and qualitative changes in epidermal stem cells (EpiSCs) and transit-amplifying (TA) cells in aged epidermis.
- To determine the impact of aging on the proliferative capacity of epidermal progenitor cells.
- To elucidate the mechanisms underlying reduced epidermal proliferation in aging.
Main Methods:
- In vivo long-term repopulation assays.
- In vitro colony formation assays.
- Analysis of keratinocyte cell cycle kinetics and growth fraction.
Main Results:
- No significant difference in epidermal stem cell (EpiSC) frequency was observed with aging.
- Aged epidermis exhibited an increased frequency of transit-amplifying (TA) cells.
- Aged TA cells persisted longer, and both aged EpiSCs and TA cells showed decreased individual proliferative capacity.
- Increased cell cycle duration and proportion of cycling keratinocytes were noted in aged epidermis.
Conclusions:
- Aging does not alter epidermal stem cell (EpiSC) frequency but increases transit-amplifying (TA) cell numbers.
- Reduced proliferative capacity per cell in aged EpiSCs and TA cells is a key feature of aging epidermis.
- The increased TA cell population may act as a compensatory mechanism for age-related decline in epidermal regenerative potential.
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