UVA and UVB Decrease the Expression of CD44 and Hyaluronate in Mouse Epidermis, which is Counteracted by Topical Retinoids

Çalıkoğlu, Emel; Sorg, Olivier; Tran, Christian; Grand, Denise; Carraux, Pierre; Saurat, Jean‐Hilaire; Kaya, Gürkan

doi:10.1562/2006-02-10-ra-801

Cited by 45 publications

(38 citation statements)

References 37 publications

(45 reference statements)

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“…12,35 In addition, it has been shown recently that UVA and UVB irradiation decrease epidermal HA and CD44 in mice. 38 In contrast only a few biochemical and histological studies addressed the effect of UV irradiation on HA content of murine and human dermis. Some studies reported increased HA content in UV-irradiated skin of mice, 39,40 whereas others reported reduced HA content.…”

Section: Discussionmentioning

confidence: 99%

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Dai

Freudenberger

Zipper

et al. 2007

The American Journal of Pathology

140

116

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Remodeling of the dermal extracellular matrix occurs during photoaging. Here, the effect of repetitive UVB irradiation on dermal hyaluronic acid (HA) was examined. C57/BL6 mice were chronically (182 days) irradiated with UVB, and consecutive skin biopsies were collected during the irradiation period and afterward (300 and 400 days of age). UVB caused marked loss of HA from the papillary dermis and down-regulation of HA synthase 1 (HAS1), HAS2, and HAS3 mRNA expression. In contrast, hyaluronidases (HYAL) 1, HYAL2, and HA receptor CD44 were unchanged. Furthermore, transforming growth factor ␤-1 (TGF-␤1) and TGF-␤1-receptor II expression were decreased in UVB-irradiated biopsies, and TGF-␤1 strongly induced HAS1 and HAS2 expression in cultured dermal fibroblasts. Therefore, TGF-␤1 might be one factor involved in UVB-induced down-regulation of HAS enzymes. In addition, total cell number and the percentage of proliferating fibroblasts in the papillary dermis of UVB-irradiated mice were decreased. Down-regulation of HAS2 by lentiviral overexpression of short hairpin RNA in vitro caused inhibition of HA synthesis, DNA synthesis, and migration of dermal fibroblasts. In conclusion, chronic UVB irradiation induces loss of HA from the dermis, thereby contributing to the quiescent phenotype of dermal fibroblasts. 1 Photoaging is the most common form of skin damage caused by chronic, repetitive sun exposure.2 The long-term exposure to solar UV irradiation induces damage to the dermal connective tissue and the extracellular matrix (ECM), which in turn leads to the aged appearance of photodamaged skin. Hallmark of this UV-induced ECM remodeling is the degradation of collagen and elastin through the UVB-induced activation of matrix metalloproteinases and decreased de novo synthesis of collagen. The mechanisms of UVB-induced matrix metalloproteinase activation 3 and inhibition of collagen synthesis have been studied in detail.2 In contrast the effect of UVB on hyaluronic acid (HA), another key component of the dermal ECM, is much less understood, and the underlying mechanisms are primarily unknown. HA is a linear polymer composed of repeating disaccharides (D-glucuronic acid-␤-1,3-N-acetylglucosamine-␤-1,4-) and assembled from the respective activated nucleotide sugars (UDPglucuronic acid, UDP-N-acetylglucosamine) at the inner plasma membrane by HA synthases (HAS). Three different HAS isoforms are known that reside in the plasma membrane and extrude the growing HA polymer into the extracellular space.4 HAS1 and HAS2 produce high molecular mass HA (2 to 4 ϫ 10 6 Da), whereas HAS3 synthesizes smaller HA (0.4 to 2.5 ϫ 10 5 Da). 5 The variation of the MW is the only modification of HA because O-or N-sulfations do not occur. HA is an agonist of CD44 and RHAMM (receptor of HA-mediated motility), which enables HA to initiate specific signaling events.6 This receptor signaling and the formation of pericellular HA coats supports proliferation and migration of a variety of cell types including skin fibroblasts. 7 In addition, antiapoptoti...

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Section: Discussionmentioning

confidence: 99%

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Dai

Freudenberger

Zipper

et al. 2007

The American Journal of Pathology

140

116

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“…We have recently shown that UVA or UVB irradiation significantly decreased the content of HA and the expression of its receptor CD44 (see below) in the epidermis of hairless mice [28]. …”

Section: Potential Mechanisms Of Skin Fragility In Dermatoporosismentioning

confidence: 99%

Dermatoporosis: A Chronic Cutaneous Insufficiency/Fragility Syndrome

Kaya

Saurat²

2007

Dermatology

Self Cite

194

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Background: Skin aging has long been considered only as a cosmetic problem. With the increase in lifespan, we are now more often experiencing a further dimension of skin aging, which is no longer only cosmetic, but also functional, in the sense that the skin has lost its protective mechanical function. Dermatoporosis is the name proposed to capture, in a holistic approach, all the aspects of this chronic cutaneous insufficiency/fragility syndrome. Observations: In this paper, we review the clinical aspects of dermatoporosis, its histological features and the current understanding of its etiological factors. The clinical manifestations of dermatoporosis comprise (i) morphologicalmarkers of fragility – rather trivial – such as senile purpura, stellate pseudoscars and skin atrophy, and (ii) functional expression of skin fragility resulting from minor traumas such as frequent skin laceration, delayed wound healing, nonhealing atrophic ulcers and subcutaneous bleeding with the formation of dissecting hematomas leading to large zones of necrosis. Dissecting hematomas bear significant morbidity needing hospitalization and urgent surgical procedures. Molecular mechanisms implying hyaluronate-CD44 pathways in the control and maintenance of epithelial growth and the viscoelastic properties of the extracellular matrix offer new opportunities for preventive intervention. Conclusion: We propose to group the different manifestations and implications of this syndrome under the umbrella term of ‘dermatoporosis’,because we think it will helpto capture the understanding of health professionals that, as osteoporosis, ‘dermatoporosis’should be prevented and treated to avoid complications. Dermatologists should be aware of this emerging syndrome and function as key players in prevention and therapy. Randomized clinical trials should demonstrate which intervention may best prevent and/or reverse dermatoporosis.

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“…Moreover, CD44 expression is reduced with exposure to UV light. This reduced expression of CD44 can be reversed by retinoids such retinol or retinaldehyde [30,31].…”

Section: Introductionmentioning

confidence: 99%

A Placebo-Controlled Study Demonstrates the Long-Lasting Anti-Aging Benefits of a Cream Containing Retinol, DihydroxyMethylChromone (DMC) and Hyaluronic Acid

Oddos¹,

Roure²,

Leyden³

et al. 2012

JCDSA

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Retinol is an ingredient used in cosmetic products for reducing the appearance of the signs of aging and photo-damage. Currently, most of these products contain 0.1% of retinol. However, at this concentration, some irritation can occur. We have evaluated in vitro and in a clinical study the potential efficacy of a combination of actives to improve the facial skin aging signs while using low concentration of retinol. We demonstrated, in vitro, that a chromone derivative, 5,7-di-hydroxy-2-methyl chromone (DMC), is able to enhance the collagen synthesis in culture of normal human dermal fibroblasts. The enhancement of retinol anti-wrinkle efficacy by DMC was confirmed in a small scale clinical trial. Specifically, a product associating low concentration of retinol (0.04%) and DMC (0.1%) in combination with low molecular weight hyaluronic acid fragments (50,000 Dalton of average molecular weight) has been applied topically for 8 weeks. Clinical results show significant improvement of various signs of facial skin aging such as wrinkles, pigmentary spots, tone unevenness, dullness and the overall photo-damage score. Improvements were still visible 4 weeks after the cessation of the test product application. This study demonstrates that significant lasting improvement of facial skin aging can be obtained with well tolerated low concentration of retinol when adequately formulated with other anti-aging ingredients.

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UVA and UVB Decrease the Expression of CD44 and Hyaluronate in Mouse Epidermis, which is Counteracted by Topical Retinoids

Cited by 45 publications

References 37 publications

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Chronic Ultraviolet B Irradiation Causes Loss of Hyaluronic Acid from Mouse Dermis Because of Down-Regulation of Hyaluronic Acid Synthases

Dermatoporosis: A Chronic Cutaneous Insufficiency/Fragility Syndrome

A Placebo-Controlled Study Demonstrates the Long-Lasting Anti-Aging Benefits of a Cream Containing Retinol, DihydroxyMethylChromone (DMC) and Hyaluronic Acid

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