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Pleiotropic age-dependent effects of mitochondrial dysfunction on epidermal stem cells
Michael C Velarde1, Marco Demaria1, Simon Melov1
1Buck Institute for Research on Aging, Novato, CA 94945.
Summary
Mitochondrial dysfunction in skin stem cells surprisingly benefits young mice by accelerating wound healing. However, it impairs skin regeneration and causes stem cell exhaustion in older mice, revealing an age-dependent role for mitochondria.
Area of Science:
- Mitochondrial Biology
- Dermatology
- Aging Research
Background:
- Aging impairs tissue homeostasis, partly due to stem/progenitor cell dysfunction.
- Mitochondrial damage is linked to accelerated aging.
- The role of mitochondrial dysfunction in epidermal stem cell aging is unclear.
Purpose of the Study:
- To investigate the hypothesis that mitochondrial dysfunction impairs epidermal stem cell renewal and function.
- To elucidate the age-dependent effects of mitochondrial dysfunction on skin homeostasis and wound healing.
Main Methods:
- Developed a mouse model with temporally controlled mitochondrial oxidative stress in epidermal stem cells via Sod2 deletion.
- Assessed wound closure, epidermal differentiation, reepithelialization, and stem cell proliferation/exhaustion.
- Utilized a tumor promoter to evaluate skin regeneration capacity.
Main Results:
- Sod2 deficiency in young mice accelerated wound closure and epidermal differentiation, despite reduced proliferation.
- In older mice, Sod2 deficiency delayed wound closure, reduced epidermal thickness, and led to stem cell exhaustion.
- Mitochondrial dysfunction in young mice mimicked age-related decline in skin regeneration when exposed to a tumor promoter.
Conclusions:
- Mitochondrial dysfunction exhibits a surprising beneficial effect on skin wound healing in young individuals.
- Mitochondrial dysfunction contributes to age-related decline in epidermal regeneration and stem cell function.
- Identified a novel age-dependent role for mitochondria in maintaining skin quality and wound healing capacity.
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