Upregulation of CD44 and Hyaluronate Synthases by Topical Retinoids in Mouse Skin

Kaya, Gürkan; Grand, Denise; Hotz, Raymonde; Augsburger, Eric; Carraux, Pierre; Didierjean, L; Saurat, J.‐H.

doi:10.1111/j.0022-202x.2004.23579.x

Cited by 32 publications

(37 citation statements)

References 27 publications

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“…Simultaneously, the mRNA levels of HAS2 and HAS3 dose-dependently increase, wheread those of HAS1 decrease 410-fold. The effect of RA on HAS2 and HAS3 expressions has been previously described (Kaya et al, 2005;Saavalainen et al, 2005); our experiments highlight downregulation of HAS1 expression concomitantly with KRT10 disappearance (Figure 1f). …”

Section: Production Of Ha By Human Keratinocytes Correlates With Exprsupporting

confidence: 83%

Hyaluronan Metabolism in Human Keratinocytes and Atopic Dermatitis Skin Is Driven by a Balance of Hyaluronan Synthases 1 and 3

Malaisse

Bourguignon

Vuyst

et al. 2014

Journal of Investigative Dermatology

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Hyaluronan (HA) is a glycosaminoglycan synthesized directly into the extracellular matrix by three hyaluronan synthases (HAS1, HAS2, and HAS3). HA is abundantly synthesized by keratinocytes but its epidermal functions remain unclear. We used culture models to grow human keratinocytes as autocrine monolayers or as reconstructed human epidermis (RHE) to assess HA synthesis and HAS expression levels during the course of keratinocyte differentiation. In both the models, epidermal differentiation downregulates HAS3 mRNA expression while increasing HAS1 without significant changes in hyaluronidase expression. HA production correlates with HAS1 mRNA expression level during normal differentiation. To investigate the regulation of HAS gene expression during inflammatory conditions linked to perturbed differentiation, lesional and non-lesional skin biopsies of atopic dermatitis (AD) patients were analyzed. HAS3 mRNA expression level increases in AD lesions compared with healthy and non-lesional skin. Simultaneously, HAS1 expression decreases. Heparin-binding EGF-like growth factor (HB-EGF) is upregulated in AD epidermis. An AD-like HAS expression pattern is observed in RHE incubated with HB-EGF. These results indicate that HAS1 is the main enzyme responsible for HA production by normal keratinocytes and thus, must be considered as an actor of normal keratinocyte differentiation. In contrast, HAS3 can be induced by HB-EGF and seems mainly involved in AD epidermis.

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Section: Production Of Ha By Human Keratinocytes Correlates With Exprsupporting

confidence: 83%

Hyaluronan Metabolism in Human Keratinocytes and Atopic Dermatitis Skin Is Driven by a Balance of Hyaluronan Synthases 1 and 3

Malaisse

Bourguignon

Vuyst

et al. 2014

Journal of Investigative Dermatology

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“…Topical treatment of the photodamaged skin with retinoic acid increases the thickness of the epidermal HA meshwork and its concentration in suction blister fluid, suggesting that HA is involved in the epidermal change induced by topical retinoic acid therapy in photodamaged skin [41]. We have recently shown that topical application of retinaldehyde upregulated the expression of CD44 and HA synthases in mouse skin [42]. …”

Section: Potential Mechanisms Of Skin Fragility In Dermatoporosismentioning

confidence: 99%

Dermatoporosis: A Chronic Cutaneous Insufficiency/Fragility Syndrome

Kaya

Saurat²

2007

Dermatology

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200

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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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“…Indeed, an up-regulation of all CD44s by retinaldehyde topically applied on mouse skin (immunohistochemical detection and northern blot) has been observed by Kaya et al and linked by these authors to the co-receptor function of this PG in heparin binding EGF receptor -mediated growth stimulation [38]. However, a moderate decrease of the total human CD44 gene transcripts has been described using a cDNA array approach when retinoids were applied in the human keratinocyte culture media, in the SkinEthic model [39].…”

Section: Discussionmentioning

confidence: 85%

Syndecans and CD44 in Normal Human Keratinocyte Cultures: Modulation with Medium Composition and All-trans Retinoic Acid

Le¹,

Callejon²,

Rodriguez³

et al. 2009

TODJ

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Abstract:We investigated chosen epidermal proteoglycans in different culture models to explore their expression by keratinocytes at various states of differentiation. Fully defined conditions of our epidermal reconstructions allowed for evaluation of the proteoglycans in "normal" or "ageing"-like epidermal tissues in vitro. The "ageing"-like epidermis was characterized by the viable layers' atrophy, low proliferation rate and premature keratinisation. Expression of all studied proteoglycan genes could be detected with quantitative real-time PCR but the syndecan-4 protein wasn't observed in the reconstructed epidermis using immunohistochemistry. Treatment with all-trans retinoic acid resulted in epithelial acanthosis, combined with up-regulation of proteoglycans in the "ageing"-like culture conditions. In "normal" reconstructed epidermis, retinoids increased the syndecan-4 gene expression but down-regulated that of syndecan-1. The observed complex changes are compatible with the presumed but still poorly understood roles of various proteoglycans in epidermal differentiation. Our defined culture models are suitable for screening of pharmacological agents modulating epidermal proteoglycan expression.

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Upregulation of CD44 and Hyaluronate Synthases by Topical Retinoids in Mouse Skin

Cited by 32 publications

References 27 publications

Hyaluronan Metabolism in Human Keratinocytes and Atopic Dermatitis Skin Is Driven by a Balance of Hyaluronan Synthases 1 and 3

Hyaluronan Metabolism in Human Keratinocytes and Atopic Dermatitis Skin Is Driven by a Balance of Hyaluronan Synthases 1 and 3

Dermatoporosis: A Chronic Cutaneous Insufficiency/Fragility Syndrome

Syndecans and CD44 in Normal Human Keratinocyte Cultures: Modulation with Medium Composition and All-trans Retinoic Acid

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