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Impaired skin wound healing in peroxisome proliferator-activated receptor (PPAR)alpha and PPARbeta mutant mice.

Michalik L, Desvergne B, Tan NS, Basu-Modak S, Escher P, Rieusset J, Peters JM, Kaya G, Gonzalez FJ, Zakany J, Metzger D, Chambon P, Duboule D, Wahli W - J. Cell Biol. (2001)

Bottom Line: Interestingly, PPARalpha and beta expression is reactivated in the adult epidermis after various stimuli, resulting in keratinocyte proliferation and differentiation such as tetradecanoylphorbol acetate topical application, hair plucking, or skin wound healing.PPARalpha is mainly involved in the early inflammation phase of the healing, whereas PPARbeta is implicated in the control of keratinocyte proliferation.In addition and very interestingly, PPARbeta mutant primary keratinocytes show impaired adhesion and migration properties.

View Article: PubMed Central - PubMed

Affiliation: Institut de Biologie Animale, Université de Lausanne, Bâtiment de Biologie, CH-1015 Lausanne, Switzerland.

ABSTRACT
We show here that the alpha, beta, and gamma isotypes of peroxisome proliferator-activated receptor (PPAR) are expressed in the mouse epidermis during fetal development and that they disappear progressively from the interfollicular epithelium after birth. Interestingly, PPARalpha and beta expression is reactivated in the adult epidermis after various stimuli, resulting in keratinocyte proliferation and differentiation such as tetradecanoylphorbol acetate topical application, hair plucking, or skin wound healing. Using PPARalpha, beta, and gamma mutant mice, we demonstrate that PPARalpha and beta are important for the rapid epithelialization of a skin wound and that each of them plays a specific role in this process. PPARalpha is mainly involved in the early inflammation phase of the healing, whereas PPARbeta is implicated in the control of keratinocyte proliferation. In addition and very interestingly, PPARbeta mutant primary keratinocytes show impaired adhesion and migration properties. Thus, the findings presented here reveal unpredicted roles for PPARalpha and beta in adult mouse epidermal repair.

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Related in: MedlinePlus

PPARα and β mutant mice are unable to sustain normal wound healing. (A–C) After excision of a full thickness skin biopsy, the surfaces of the healing wounds were measured over time on wild-type (+/+), heterozygous (+/−), or  (−/−) mice: PPARγ (A), PPARα (B), and PPARβ (C). The surfaces are plotted as a percentage of the surface of the wound at day zero (± SEM, n = 8–10). Asterisks indicate that the difference is statistically significant (asterisk, P < 0.05; double asterisk, P < 0.01). Arrows indicate the mean time for complete healing of the wild-type control mice (black lozenge) or transgenic mice (grey square).
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fig6: PPARα and β mutant mice are unable to sustain normal wound healing. (A–C) After excision of a full thickness skin biopsy, the surfaces of the healing wounds were measured over time on wild-type (+/+), heterozygous (+/−), or (−/−) mice: PPARγ (A), PPARα (B), and PPARβ (C). The surfaces are plotted as a percentage of the surface of the wound at day zero (± SEM, n = 8–10). Asterisks indicate that the difference is statistically significant (asterisk, P < 0.05; double asterisk, P < 0.01). Arrows indicate the mean time for complete healing of the wild-type control mice (black lozenge) or transgenic mice (grey square).

Mentions: The PPARγ+/− heterozygous mice were not different from wild-type littermates in their wound-healing process (Fig. 6 A), which is consistent with PPARγ being hardly detectable after injury.


Impaired skin wound healing in peroxisome proliferator-activated receptor (PPAR)alpha and PPARbeta mutant mice.

Michalik L, Desvergne B, Tan NS, Basu-Modak S, Escher P, Rieusset J, Peters JM, Kaya G, Gonzalez FJ, Zakany J, Metzger D, Chambon P, Duboule D, Wahli W - J. Cell Biol. (2001)

PPARα and β mutant mice are unable to sustain normal wound healing. (A–C) After excision of a full thickness skin biopsy, the surfaces of the healing wounds were measured over time on wild-type (+/+), heterozygous (+/−), or  (−/−) mice: PPARγ (A), PPARα (B), and PPARβ (C). The surfaces are plotted as a percentage of the surface of the wound at day zero (± SEM, n = 8–10). Asterisks indicate that the difference is statistically significant (asterisk, P < 0.05; double asterisk, P < 0.01). Arrows indicate the mean time for complete healing of the wild-type control mice (black lozenge) or transgenic mice (grey square).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196455&req=5

fig6: PPARα and β mutant mice are unable to sustain normal wound healing. (A–C) After excision of a full thickness skin biopsy, the surfaces of the healing wounds were measured over time on wild-type (+/+), heterozygous (+/−), or (−/−) mice: PPARγ (A), PPARα (B), and PPARβ (C). The surfaces are plotted as a percentage of the surface of the wound at day zero (± SEM, n = 8–10). Asterisks indicate that the difference is statistically significant (asterisk, P < 0.05; double asterisk, P < 0.01). Arrows indicate the mean time for complete healing of the wild-type control mice (black lozenge) or transgenic mice (grey square).
Mentions: The PPARγ+/− heterozygous mice were not different from wild-type littermates in their wound-healing process (Fig. 6 A), which is consistent with PPARγ being hardly detectable after injury.

Bottom Line: Interestingly, PPARalpha and beta expression is reactivated in the adult epidermis after various stimuli, resulting in keratinocyte proliferation and differentiation such as tetradecanoylphorbol acetate topical application, hair plucking, or skin wound healing.PPARalpha is mainly involved in the early inflammation phase of the healing, whereas PPARbeta is implicated in the control of keratinocyte proliferation.In addition and very interestingly, PPARbeta mutant primary keratinocytes show impaired adhesion and migration properties.

View Article: PubMed Central - PubMed

Affiliation: Institut de Biologie Animale, Université de Lausanne, Bâtiment de Biologie, CH-1015 Lausanne, Switzerland.

ABSTRACT
We show here that the alpha, beta, and gamma isotypes of peroxisome proliferator-activated receptor (PPAR) are expressed in the mouse epidermis during fetal development and that they disappear progressively from the interfollicular epithelium after birth. Interestingly, PPARalpha and beta expression is reactivated in the adult epidermis after various stimuli, resulting in keratinocyte proliferation and differentiation such as tetradecanoylphorbol acetate topical application, hair plucking, or skin wound healing. Using PPARalpha, beta, and gamma mutant mice, we demonstrate that PPARalpha and beta are important for the rapid epithelialization of a skin wound and that each of them plays a specific role in this process. PPARalpha is mainly involved in the early inflammation phase of the healing, whereas PPARbeta is implicated in the control of keratinocyte proliferation. In addition and very interestingly, PPARbeta mutant primary keratinocytes show impaired adhesion and migration properties. Thus, the findings presented here reveal unpredicted roles for PPARalpha and beta in adult mouse epidermal repair.

Show MeSH
Related in: MedlinePlus