Retinoic acid improves epidermal morphogenesis

Asselineau, Daniel; Bernard, Bruno; Bailly, Catherine; Darmon, Michaël

doi:10.1016/0012-1606(89)90037-7

Cited by 231 publications

(111 citation statements)

References 47 publications

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“…While it is generally accepted that retinoids inhibit ter minal differentiation in the epidermis, it has only recently been suggested that retinoids also act to enhance certain features of the differentiated process (Asselineau et al, 1989). This notion has been supported by examining the behavior of keratinocyte lines expressing a truncated RARy capable of suppressing action at retinoid response elements (Aneskievich and Fuchs, 1992).…”

Section: Retinoidsmentioning

confidence: 99%

Epidermal differentiation and keratin gene expression

Fuchs

1993

Journal of Cell Science

157

101

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SUMMARYThe epidermis of the skin is a stratified squamous epithelium, which plays an important protective role. It manifests this role by building an extensive cytoskeletal architecture, the unique feature of which is the presence of keratin filaments. There are two major pairs of ker atins in the epidermis: one pair is expressed in dividing cells and the other expressed in terminally differentiat ing cells. As such, keratins provide useful biochemical markers to explore the molecular mechanisms underly-

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Section: Retinoidsmentioning

confidence: 99%

Epidermal differentiation and keratin gene expression

Fuchs

1993

Journal of Cell Science

157

101

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“…AP-1 has been put forward as a key transcriptional regulator of genes encoding several keratinocyte differentiation proteins, e.g. keratin 1, transglutaminase 1 (Tgm1), loricrin and involucrin (see [27] and references therein), all of which are repressed by RA [28,29]. In support of this theory, the DNA-binding activity of AP-1 was recently found to increase in cultured keratinocytes induced to differentiate by elevated extracellular calcium [30].…”

Section: Introductionmentioning

confidence: 97%

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

Karlsson¹,

Vahlquist²,

Törmä³

2010

Journal of Dermatological Science

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This is an author produced version of a paper published in Journal ofDermatological Science. This paper has been peer-reviewed but does not include the final publisher proof-corrections or journal pagination. Access to the published version may require subscription. Published with permission from: ElsevierThe final publication is available at www.elsevier.com Conclusions:Retinoid signalling is profoundly altered upon differentiation of keratinocytes and the effects depend on how cellular differentiation is initiated.

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“…On this dermal support a full thickness epidermis can be reconstructed, that displays normal keratinocyte differentiation markers and horny layers (Asselineau et al, 1985;1989). This skin model is suitable not only for evaluating the effects of pharmacological agents, such as retinoids (Asselineau et al, 1989;Asselineau and Darmon, 1995;Magnaldo et al, 1992) but also the response to environmental stimuli. This system was recently used to study the typical early DNA damages induced in epidermis by UVB as well as the subsequent recovery phase (Bernerd and Asselineau, 1997).…”

Section: Introductionmentioning

confidence: 99%

UVA exposure of human skin reconstructed in vitro induces apoptosis of dermal fibroblasts: subsequent connective tissue repair and implications in photoaging

1998

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The skin reconstructed in vitro has been previously shown to be a useful model to investigate the effects of UVB exposure (Bernerd and Asselineau, 1997). The present study describes the response to UVA irradiation. Major alterations were observed within the dermal compartment. Apoptosis of fibroblasts located in the superficial area of the dermal equivalent was observed as soon as 6 h after irradiation, leading to their disappearance after 48 h. This effect was obtained without major alterations of epidermal keratinocytes suggesting a differential cell type sensitivity to UVA radiations. In addition, collagenase I was secreted by dermal fibroblasts. The UVA dermal effects could be observed even after removal of the epidermis during the post irradiation period, demonstrating that they were independent of the keratinocyte response. The analysis of the tissue regeneration during the following 2 weeks revealed a connective tissue repair via fibroblasts proliferation, migration and active synthesis of extracellular matrix proteins such as fibronectin and procollagen I. This cellular recolonization of the superficial part of the dermal equivalent was due to activation of surviving fibroblasts located deeply in the dermal equivalent. The direct damage in the dermis and the subsequent connective tissue repair may contribute to the formation of UVA-induced dermal alterations.

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Retinoic acid improves epidermal morphogenesis

Cited by 231 publications

References 47 publications

Epidermal differentiation and keratin gene expression

Epidermal differentiation and keratin gene expression

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

UVA exposure of human skin reconstructed in vitro induces apoptosis of dermal fibroblasts: subsequent connective tissue repair and implications in photoaging

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