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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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Related in: MedlinePlus

Interfollicular epidermal proliferation declines with aging. (A, B) Representative young (A) and old (B) epidermal whole mounts stained for keratin 14 (green) plus Ki67 (red). (C) Quantification of Ki67(+) nuclei per interfollicular epidermis unit (defined in Silva-Vargas et al., 2005) in young and old mice. (D–F) Flow cytometric analysis of total (left side graphs, C–E) or α6(+) keratinocyte (right side graphs, C–E) cell cycle status in young (green) versus old (red) skin preparations. (G, H) Keratin 15 (green) plus Ki67 (red) immunostaining in young and old mice to determine bulge stem-cell-specific proliferation. (I) Quantification of Ki67(+) cells per bulge in young and old mice. Scale bars (A, B) = 100 µm. (n = 4 mice/age; *P < 0.05).
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fig03: Interfollicular epidermal proliferation declines with aging. (A, B) Representative young (A) and old (B) epidermal whole mounts stained for keratin 14 (green) plus Ki67 (red). (C) Quantification of Ki67(+) nuclei per interfollicular epidermis unit (defined in Silva-Vargas et al., 2005) in young and old mice. (D–F) Flow cytometric analysis of total (left side graphs, C–E) or α6(+) keratinocyte (right side graphs, C–E) cell cycle status in young (green) versus old (red) skin preparations. (G, H) Keratin 15 (green) plus Ki67 (red) immunostaining in young and old mice to determine bulge stem-cell-specific proliferation. (I) Quantification of Ki67(+) cells per bulge in young and old mice. Scale bars (A, B) = 100 µm. (n = 4 mice/age; *P < 0.05).

Mentions: To determine whether epidermal proliferation was altered in aged skin, we performed whole-mount immunostaining for Ki67 and keratin 14 (Fig. 3A,B). Proliferation of each unit of interfollicular epidermis (IFE) (as defined by Silva-Vargas et al., 2005) appeared to decrease in all aged skin samples, although this was not statistically significant (P < 0.09; Fig. 3C). Tail whole-mount labelling for Ki67 revealed that there were no differences in K15 positive, bulge-associated stem cell proliferation between young and old samples (yellow arrowheads, Fig. 3G–I). Nevertheless, flow cytometry revealed an increase in G1 phase cells concomitant with reductions in S and G2/M-phase cells in aged telogen-phase skin [total or α6(+) keratinocytes; Fig. 3D–F]. This is consistent with a modest decrease in proliferation with age.


Epidermal stem cells are retained in vivo throughout skin aging.

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

Interfollicular epidermal proliferation declines with aging. (A, B) Representative young (A) and old (B) epidermal whole mounts stained for keratin 14 (green) plus Ki67 (red). (C) Quantification of Ki67(+) nuclei per interfollicular epidermis unit (defined in Silva-Vargas et al., 2005) in young and old mice. (D–F) Flow cytometric analysis of total (left side graphs, C–E) or α6(+) keratinocyte (right side graphs, C–E) cell cycle status in young (green) versus old (red) skin preparations. (G, H) Keratin 15 (green) plus Ki67 (red) immunostaining in young and old mice to determine bulge stem-cell-specific proliferation. (I) Quantification of Ki67(+) cells per bulge in young and old mice. Scale bars (A, B) = 100 µm. (n = 4 mice/age; *P < 0.05).
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fig03: Interfollicular epidermal proliferation declines with aging. (A, B) Representative young (A) and old (B) epidermal whole mounts stained for keratin 14 (green) plus Ki67 (red). (C) Quantification of Ki67(+) nuclei per interfollicular epidermis unit (defined in Silva-Vargas et al., 2005) in young and old mice. (D–F) Flow cytometric analysis of total (left side graphs, C–E) or α6(+) keratinocyte (right side graphs, C–E) cell cycle status in young (green) versus old (red) skin preparations. (G, H) Keratin 15 (green) plus Ki67 (red) immunostaining in young and old mice to determine bulge stem-cell-specific proliferation. (I) Quantification of Ki67(+) cells per bulge in young and old mice. Scale bars (A, B) = 100 µm. (n = 4 mice/age; *P < 0.05).
Mentions: To determine whether epidermal proliferation was altered in aged skin, we performed whole-mount immunostaining for Ki67 and keratin 14 (Fig. 3A,B). Proliferation of each unit of interfollicular epidermis (IFE) (as defined by Silva-Vargas et al., 2005) appeared to decrease in all aged skin samples, although this was not statistically significant (P < 0.09; Fig. 3C). Tail whole-mount labelling for Ki67 revealed that there were no differences in K15 positive, bulge-associated stem cell proliferation between young and old samples (yellow arrowheads, Fig. 3G–I). Nevertheless, flow cytometry revealed an increase in G1 phase cells concomitant with reductions in S and G2/M-phase cells in aged telogen-phase skin [total or α6(+) keratinocytes; Fig. 3D–F]. This is consistent with a modest decrease in proliferation with age.

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