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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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Igfbp3 does not directly influence epidermal immune cell abundance but results in increased anagen follicles. (A, B) Representative whole mounts from age- and sex-matched wild-type (WT) (A) and Igfbp3KO (B) tail epidermis immunolabelled for keratin 14 (green) and CD45 (red). (C) Quantification of CD45 cell abundance in WT and knock-out (KO) epidermis per square millimetre. (D, E) WT (D) and KO (E) whole mounts stained for γδTCR (green) and CD3 (red) identify CD3(+) T cells and dendritic epidermal T cells (orange). (F) Quantification of CD3(+) and γδTCR(+) cell abundance in WT and KO skin. (G, H) WT (G) and KO (H) tail whole mounts stained for keratin 15 (green) and Ki67 (red) to identify bulge stem cells and mitotic keratinocytes, respectively. (I) Quantification of percentage of total growing (anagen) follicles present in WT and KO tail epidermal whole mounts (e.g. see arrowheads, H). Scale bars = 100 µm (A, B, D, E, G, H). (n = 4 mice/genotype; *P < 0.05; I).
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fig06: Igfbp3 does not directly influence epidermal immune cell abundance but results in increased anagen follicles. (A, B) Representative whole mounts from age- and sex-matched wild-type (WT) (A) and Igfbp3KO (B) tail epidermis immunolabelled for keratin 14 (green) and CD45 (red). (C) Quantification of CD45 cell abundance in WT and knock-out (KO) epidermis per square millimetre. (D, E) WT (D) and KO (E) whole mounts stained for γδTCR (green) and CD3 (red) identify CD3(+) T cells and dendritic epidermal T cells (orange). (F) Quantification of CD3(+) and γδTCR(+) cell abundance in WT and KO skin. (G, H) WT (G) and KO (H) tail whole mounts stained for keratin 15 (green) and Ki67 (red) to identify bulge stem cells and mitotic keratinocytes, respectively. (I) Quantification of percentage of total growing (anagen) follicles present in WT and KO tail epidermal whole mounts (e.g. see arrowheads, H). Scale bars = 100 µm (A, B, D, E, G, H). (n = 4 mice/genotype; *P < 0.05; I).

Mentions: In order to determine whether altered Igfbp3 expression directly influenced epidermal proliferation or peripheral immunity, we compared these properties in tail epidermal whole mounts from wild-type (WT) and Igfbp3 knock-out (KO) mice (Ning et al., 2006). Total haematopoietic cell (CD45; Fig. 6A–C), and T and DETC cell abundance (CD3 and γδTCR; Fig. 6D–F) were unchanged in Igfbp3KO compared to WT mouse skin. There were also no differences in stem cell abundance, interfollicular proliferation, and follicle patterning (Fig. 6G,H; data not shown). However, the proportion of anagen-phase follicles was significantly increased in Igfbp3KO mice compared with WT controls (Fig. 6I; arrowheads Fig. 6H). These results indicate that although peripheral immunity and interfollicular proliferation decline in conjunction with reduced Igfbp3 expression during aging, these events are not causally linked.


Epidermal stem cells are retained in vivo throughout skin aging.

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

Igfbp3 does not directly influence epidermal immune cell abundance but results in increased anagen follicles. (A, B) Representative whole mounts from age- and sex-matched wild-type (WT) (A) and Igfbp3KO (B) tail epidermis immunolabelled for keratin 14 (green) and CD45 (red). (C) Quantification of CD45 cell abundance in WT and knock-out (KO) epidermis per square millimetre. (D, E) WT (D) and KO (E) whole mounts stained for γδTCR (green) and CD3 (red) identify CD3(+) T cells and dendritic epidermal T cells (orange). (F) Quantification of CD3(+) and γδTCR(+) cell abundance in WT and KO skin. (G, H) WT (G) and KO (H) tail whole mounts stained for keratin 15 (green) and Ki67 (red) to identify bulge stem cells and mitotic keratinocytes, respectively. (I) Quantification of percentage of total growing (anagen) follicles present in WT and KO tail epidermal whole mounts (e.g. see arrowheads, H). Scale bars = 100 µm (A, B, D, E, G, H). (n = 4 mice/genotype; *P < 0.05; I).
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2339763&req=5

fig06: Igfbp3 does not directly influence epidermal immune cell abundance but results in increased anagen follicles. (A, B) Representative whole mounts from age- and sex-matched wild-type (WT) (A) and Igfbp3KO (B) tail epidermis immunolabelled for keratin 14 (green) and CD45 (red). (C) Quantification of CD45 cell abundance in WT and knock-out (KO) epidermis per square millimetre. (D, E) WT (D) and KO (E) whole mounts stained for γδTCR (green) and CD3 (red) identify CD3(+) T cells and dendritic epidermal T cells (orange). (F) Quantification of CD3(+) and γδTCR(+) cell abundance in WT and KO skin. (G, H) WT (G) and KO (H) tail whole mounts stained for keratin 15 (green) and Ki67 (red) to identify bulge stem cells and mitotic keratinocytes, respectively. (I) Quantification of percentage of total growing (anagen) follicles present in WT and KO tail epidermal whole mounts (e.g. see arrowheads, H). Scale bars = 100 µm (A, B, D, E, G, H). (n = 4 mice/genotype; *P < 0.05; I).
Mentions: In order to determine whether altered Igfbp3 expression directly influenced epidermal proliferation or peripheral immunity, we compared these properties in tail epidermal whole mounts from wild-type (WT) and Igfbp3 knock-out (KO) mice (Ning et al., 2006). Total haematopoietic cell (CD45; Fig. 6A–C), and T and DETC cell abundance (CD3 and γδTCR; Fig. 6D–F) were unchanged in Igfbp3KO compared to WT mouse skin. There were also no differences in stem cell abundance, interfollicular proliferation, and follicle patterning (Fig. 6G,H; data not shown). However, the proportion of anagen-phase follicles was significantly increased in Igfbp3KO mice compared with WT controls (Fig. 6I; arrowheads Fig. 6H). These results indicate that although peripheral immunity and interfollicular proliferation decline in conjunction with reduced Igfbp3 expression during aging, these events are not causally linked.

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