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Epidermal stem cells are retained in vivo throughout skin aging.

Giangreco A, Qin M, Pintar JE, Watt FM - Aging Cell (2008)

Bottom Line: In healthy individuals, skin integrity is maintained by epidermal stem cells which self-renew and generate daughter cells that undergo terminal differentiation.It is currently unknown whether epidermal stem cells influence or are affected by skin aging.We therefore compared young and aged skin stem cell abundance, organization, and proliferation.

View Article: PubMed Central - PubMed

Affiliation: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK. adam.giangreco@cancer.org.uk

ABSTRACT
In healthy individuals, skin integrity is maintained by epidermal stem cells which self-renew and generate daughter cells that undergo terminal differentiation. It is currently unknown whether epidermal stem cells influence or are affected by skin aging. We therefore compared young and aged skin stem cell abundance, organization, and proliferation. We discovered that despite age-associated differences in epidermal proliferation, dermal thickness, follicle patterning, and immune cell abundance, epidermal stem cells were maintained at normal levels throughout life. These findings, coupled with observed dermal gene expression changes, suggest that epidermal stem cells themselves are intrinsically aging resistant and that local environmental or systemic factors modulate skin aging.

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Age-associated changes in murine skin. (A, B) Haematoxylin-and-eosin-stained sections of young (A) and old (B) telogen murine dorsal skin showing epidermis, dermis, hypodermis, and underlying muscle. Abnormal follicular architecture, dermal thinning, and hypodermal thickening are present in aged skin. (C, D) Keratin 14-stained skin whole-mount images from young (C) and old (D) mice [bracket indicates hair follicle (HF) bulge]. (E) Average dermis (measured from epidermis to hypodermis) and hypodermis (measured from dermis to underlying muscle) thickness in young (green) and old (red) mice. (F) Average number of HFs per cluster in young (green) and old (red) tail epidermis. (G) Quantitative polymerase chain reaction analysis of p16/Ink4a/Arf gene expression in skin of mice of increasing age. Scale bars = 100 µm (A, B, D, E). (n = 4 mice/age; *P < 0.05).
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fig01: Age-associated changes in murine skin. (A, B) Haematoxylin-and-eosin-stained sections of young (A) and old (B) telogen murine dorsal skin showing epidermis, dermis, hypodermis, and underlying muscle. Abnormal follicular architecture, dermal thinning, and hypodermal thickening are present in aged skin. (C, D) Keratin 14-stained skin whole-mount images from young (C) and old (D) mice [bracket indicates hair follicle (HF) bulge]. (E) Average dermis (measured from epidermis to hypodermis) and hypodermis (measured from dermis to underlying muscle) thickness in young (green) and old (red) mice. (F) Average number of HFs per cluster in young (green) and old (red) tail epidermis. (G) Quantitative polymerase chain reaction analysis of p16/Ink4a/Arf gene expression in skin of mice of increasing age. Scale bars = 100 µm (A, B, D, E). (n = 4 mice/age; *P < 0.05).

Mentions: In order to determine whether murine skin exhibited any overt changes with increased age, we obtained young (2–6 months) and old (22–26 months) adult C57/Bl6 mice from the National Institute of Health (NIH) and an in-house colony. Telogen-phase mouse dorsal skin from 24-month-old to 26-month-old mice presented significantly decreased dermal cellularity and thickness, while the subcutaneous adipose layer (hypodermis) was increased relative to young telogen-phase dorsal skin (Fig. 1A,B,E). The total dermal plus hypodermal thickness was similar in young and old skin, raising the possibility that dermal to hypodermal conversion had occurred (Fig. 1E).


Epidermal stem cells are retained in vivo throughout skin aging.

Giangreco A, Qin M, Pintar JE, Watt FM - Aging Cell (2008)

Age-associated changes in murine skin. (A, B) Haematoxylin-and-eosin-stained sections of young (A) and old (B) telogen murine dorsal skin showing epidermis, dermis, hypodermis, and underlying muscle. Abnormal follicular architecture, dermal thinning, and hypodermal thickening are present in aged skin. (C, D) Keratin 14-stained skin whole-mount images from young (C) and old (D) mice [bracket indicates hair follicle (HF) bulge]. (E) Average dermis (measured from epidermis to hypodermis) and hypodermis (measured from dermis to underlying muscle) thickness in young (green) and old (red) mice. (F) Average number of HFs per cluster in young (green) and old (red) tail epidermis. (G) Quantitative polymerase chain reaction analysis of p16/Ink4a/Arf gene expression in skin of mice of increasing age. Scale bars = 100 µm (A, B, D, E). (n = 4 mice/age; *P < 0.05).
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Related In: Results  -  Collection

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fig01: Age-associated changes in murine skin. (A, B) Haematoxylin-and-eosin-stained sections of young (A) and old (B) telogen murine dorsal skin showing epidermis, dermis, hypodermis, and underlying muscle. Abnormal follicular architecture, dermal thinning, and hypodermal thickening are present in aged skin. (C, D) Keratin 14-stained skin whole-mount images from young (C) and old (D) mice [bracket indicates hair follicle (HF) bulge]. (E) Average dermis (measured from epidermis to hypodermis) and hypodermis (measured from dermis to underlying muscle) thickness in young (green) and old (red) mice. (F) Average number of HFs per cluster in young (green) and old (red) tail epidermis. (G) Quantitative polymerase chain reaction analysis of p16/Ink4a/Arf gene expression in skin of mice of increasing age. Scale bars = 100 µm (A, B, D, E). (n = 4 mice/age; *P < 0.05).
Mentions: In order to determine whether murine skin exhibited any overt changes with increased age, we obtained young (2–6 months) and old (22–26 months) adult C57/Bl6 mice from the National Institute of Health (NIH) and an in-house colony. Telogen-phase mouse dorsal skin from 24-month-old to 26-month-old mice presented significantly decreased dermal cellularity and thickness, while the subcutaneous adipose layer (hypodermis) was increased relative to young telogen-phase dorsal skin (Fig. 1A,B,E). The total dermal plus hypodermal thickness was similar in young and old skin, raising the possibility that dermal to hypodermal conversion had occurred (Fig. 1E).

Bottom Line: In healthy individuals, skin integrity is maintained by epidermal stem cells which self-renew and generate daughter cells that undergo terminal differentiation.It is currently unknown whether epidermal stem cells influence or are affected by skin aging.We therefore compared young and aged skin stem cell abundance, organization, and proliferation.

View Article: PubMed Central - PubMed

Affiliation: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK. adam.giangreco@cancer.org.uk

ABSTRACT
In healthy individuals, skin integrity is maintained by epidermal stem cells which self-renew and generate daughter cells that undergo terminal differentiation. It is currently unknown whether epidermal stem cells influence or are affected by skin aging. We therefore compared young and aged skin stem cell abundance, organization, and proliferation. We discovered that despite age-associated differences in epidermal proliferation, dermal thickness, follicle patterning, and immune cell abundance, epidermal stem cells were maintained at normal levels throughout life. These findings, coupled with observed dermal gene expression changes, suggest that epidermal stem cells themselves are intrinsically aging resistant and that local environmental or systemic factors modulate skin aging.

Show MeSH
Related in: MedlinePlus