Effect of topical retinoic acid on the interleukin Iα and β immunoreactive pool in normal human epidermis

Gruaz, Dominique; Didierjean, Liliane; Gumowski‐Sunek, D.; Saurat, J.‐H.

doi:10.1111/j.1365-2133.1990.tb06286.x

Cited by 15 publications

(7 citation statements)

References 13 publications

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“…However, when IL‐1α and TNF‐α were examined at the mRNA level, the former cytokine was found to be downregulated in talarozole‐treated skin. In previous studies of ATRA‐treated skin no change of IL‐1α expression was observed 45,46 …”

Section: Discussionmentioning

confidence: 89%

Topical treatment with CYP26 inhibitor talarozole (R115866) dose dependently alters the expression of retinoid-regulated genes in normal human epidermis

Loriè

Cools²,

Borgers³

et al. 2009

British Journal of Dermatology

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Section: Discussionmentioning

confidence: 89%

Topical treatment with CYP26 inhibitor talarozole (R115866) dose dependently alters the expression of retinoid-regulated genes in normal human epidermis

Loriè

Cools²,

Borgers³

et al. 2009

British Journal of Dermatology

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“…The treatment of RHE with retinoic acid strongly upregulated IL‐1‐α transcripts and increased also those for IL‐1RA, but to a lower extent; IL‐1‐β transcripts were not significantly detected. This response could be assimilated to the known pro‐inflammatory activity of retinoic acid (13,14); however, interesting observations are that (1) the positive IL‐1 receptor is apparently not upregulated and above all, (2) the negative and soluble IL‐1 receptor (IL‐1RII) is strongly over‐expressed. Based on these results, we could hypothesize that both untreated and retinoic acid‐treated epidermal keratinocytes protect themselves from the IL‐1 they produce.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to these direct receptor‐mediated transcriptional effects, retinoids are known to have pro‐inflammatory activities (13), leading to the production of specific cytokines, which induce secondary responses in terms of gene expression (14). All these effects result in a complex pattern of transcriptional responses, which are thought to be specific for retinoids.…”

Section: Introductionmentioning

confidence: 99%

Comparison of gene expression profiles in human keratinocyte mono‐layer cultures, reconstituted epidermis and normal human skin; transcriptional effects of retinoid treatments in reconstituted human epidermis

Bernard¹,

Pedretti²,

Rosdy

et al. 2002

Experimental Dermatology

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In order to validate a model for predictive screening of dermatological drugs, we used a customized cDNA macro-array system containing 475 skin-related genes to analyze the gene expression patterns in human keratinocytes from different origins: (1) normal human epidermal keratinocyte mono-layer cultures, (2) the commercially available SkinEthic reconstituted human epidermis model, and (3) biopsies of normal human epidermis. Few markers of those that were detected significantly in keratinocyte mono-layers or in reconstituted epidermis were undetected or detected at very low level in the normal epidermis biopsies. A comparative expression of more than 100 markers could be evidenced in both normal epidermis and reconstituted epidermis samples; however, only 90% of these were detected in keratinocyte mono-layers: expression of several terminal differentiation markers, such as filaggrin, loricrin, and corneodesmosin were strongly detected in normal epidermis and reconstituted epidermis, but were not significantly expressed in keratinocyte mono-layers. Under the experimental conditions described herein, the reconstituted human epidermis model was found to significantly reproduce the gene expression profile of normal human epidermis. Using the same methodology, we then investigated the effects of all-trans retinoic acid, 9-cis retinoic acid, all-trans retinol and a commercialized tretinoin-containing cream (Retacnyl) on the gene expression profiles of reconstituted human epidermis. According to the nature and the length of the treatments, more than 40 genes were found significantly modified. Among the genes whose expression was decreased, we found cytokeratins 1, 10, 2E, and 6B, several cornified envelope precursors, integrins alpha 3, alpha 6, beta 1, beta 4, some components of desmosomes, of hemi-desmosomes and of the epidermal basement membrane. Transcriptional upregulation was observed for keratins 18 and 19, autocrine and paracrine growth factors such as HB-EGF, IGF 1, PDGF-A, calgranulins A and B, interleukin-1 alpha and the other IL-1-related markers, type II IL-1 receptor and type I IL-1-receptor antagonist. Our results confirm most of the known effects of retinoids on human epidermis, but also give new insights into their complex pharmacological activity on skin. The reconstituted human epidermis used proves to be a highly predictive model for efficacy evaluation of skin-targeted compounds, such as retinoids.

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“…for longer than the time necessary for the induction of the biological effects due to topical retinoids [14,15], 2.) The absence of erythema does not imply that there was no biological effect since it has been clearly shown that significant bio logical responses do occur even when no irritation is detectable [16]; this has been already discussed else where [17].…”

Section: Discussionmentioning

confidence: 99%

Topical Retinoic Acid Does Not Alter the Vasoconstrictive Properties of Topical Corticosteroids in Humans

Schmied

Saurat²

1991

Dermatology

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Dermo-epidermal atrophy is one of the main side effects of long-term treatment with topical corticosteroids. Retinoic acid may prevent and even reverse these effects in animals. Extension of this concept to therapy in humans implies that several studies have been performed; among others, it has to be established that treatment with topical retinoic acid does not interfere with the anti-inflammatory action of topical corticosteroids. The present study on the cutaneous vasoconstriction test comprised two different double-blind approaches: (i) vasoconstriction tests with betamethasone dipropionate (Diprolene®) and clobetasone butyrate (Emovate®) were carried out on skin that had previously been treated for 10 days with retinoic acid 0.01 0.025 or 0.05% (or excipient); (ii) vasoconstriction tests with a combination of triamcinolone acetonide 0.1% and retinoic acid 0.025% were compared with triamcinolone acetonide 0.1% alone. Pretreatment for 10 days with retinoic acid did not alter the vasoconstriction induced by corticosteroids: no decrease or increase in the vasoconstriction score was observed, whether the skin had been previously treated with retinoic acid or with excipient. The vasoconstriction scores obtained with a combination of retinoic acid and triamcinolone acetonide were identical with those obtained with the steroid alone. This study indicates that retinoic acid does not inhibit the vasoconstriction induced by topical corticosteroids and suggests that the anti-inflammatory effect of the latter should be maintained in association with retinoic acid.

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Effect of topical retinoic acid on the interleukin Iα and β immunoreactive pool in normal human epidermis

Cited by 15 publications

References 13 publications

Topical treatment with CYP26 inhibitor talarozole (R115866) dose dependently alters the expression of retinoid-regulated genes in normal human epidermis

Topical treatment with CYP26 inhibitor talarozole (R115866) dose dependently alters the expression of retinoid-regulated genes in normal human epidermis

Comparison of gene expression profiles in human keratinocyte mono‐layer cultures, reconstituted epidermis and normal human skin; transcriptional effects of retinoid treatments in reconstituted human epidermis

Topical Retinoic Acid Does Not Alter the Vasoconstrictive Properties of Topical Corticosteroids in Humans

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