Category Archives: Exp Dermatol

Fullerene C60 with cytoprotective and cytotoxic potential: prospects as a novel treatment agent in Dermatology?

Fullerene C60 with cytoprotective and cytotoxic potential: prospects as a novel treatment agent in Dermatology?

Exp Dermatol. 2016 Aug 19;

Authors: Rondags A, Yuen WY, Jonkman MF, Horváth B

Abstract
Fullerenes, discovered in 1985, form the third major carbon allotrope besides diamond and graphite.(1,2) They exclusively exist out of n-three-coordinate carbon atoms that are arranged in exactly12 pentagons and (n/2-10) hexagons, where n ≥ 20, forming hollow spheres, tubes, and other shapes.(2) In 1990, the synthesis of macroscopic (milligrams) amounts of fullerenes through resistive heating of graphite began to develop.(3) Because it appeared that fullerenes possessed many unique and attractive physiochemical properties, such as light weight, high tensile strength, thermal/chemical stability and conductivity, the possibilities of these carbon molecules have been extensively explored in many fields of science. The discovery of fullerenes was considered of great importance and has strongly influenced the field of chemistry, which therefore resulted in an award of the Nobel Prize in Chemistry to the discoverers of fullerenes in 1996. This article is protected by copyright. All rights reserved.

PMID: 27541937 [PubMed – as supplied by publisher]

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Phenotypic variation in epidermolytic ichthyosis: clinical and functional evaluation of the novel p.(Met339Lys) mutation in the L12 domain of KRT1.

Phenotypic variation in epidermolytic ichthyosis: clinical and functional evaluation of the novel p.(Met339Lys) mutation in the L12 domain of KRT1.

Exp Dermatol. 2015 Jun 29;

Authors: Nellen RG, Nagtzaam IF, Hoogeboom AJ, Bladergroen RS, Jonkman MF, Steijlen PM, van Steensel MA, van Geel M

Abstract
Epidermolytic ichthyosis (EI) is an autosomal dominant skin disorder caused by mutations in KRT1 and KRT10(1), encoding keratins 1 (K1) and 10 (K10)(2) which are the major components of the intermediate filament cytoskeleton in keratinocytes of the stratum spinosum. There is extensive phenotypic variation in patients harboring a KRT1 mutation, with a strong genotype-phenotype correlation having been reported. Severe phenotypes (neonatal erythroderma and blistering, generalized ichthyosis) are caused by mutations in the helix boundary motifs (HBM) of K1(1, 3). Mutations causing milder phenotypes (palmoplantar keratoderma (PPK), mild blistering, absence of ichthyosis and erythroderma) occur in the central α-helical region (1B, 2B)(3) and linker (L12) domain(4, 5). However, exceptions to this rule have been reported(3). In addition to this observation, we report the first family with phenotypes of varying severity of EI caused by the same mutation in the L12 domain of K1. This article is protected by copyright. All rights reserved.

PMID: 26120802 [PubMed – as supplied by publisher]

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Pigmentation and melanocyte supply to the epidermis depend on type XVII collagen.

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Pigmentation and melanocyte supply to the epidermis depend on type XVII collagen.

Exp Dermatol. 2013 Dec 11;

Authors: Gostyński A, Pasmooij AM, Del Rio M, Diercks GF, Pas HH, Jonkman MF

Abstract
Genetic deficiency of type XVII collagen (C17), laminin-332, or type VII collagen causes epidermolysis bullosa (EB). Spontaneous correction of the deficiency, also known as revertant mosaicism, is caused by a second somatic mutation that restores protein expression resulting in clinically healthy (revertant) patches surrounded by fragile (mutant) skin. Interestingly, in some patients patches of revertant skin show hyperpigmentation. To study the possible role of affected proteins in pigmentation and melanocyte distribution, we investigated clinical documentation and skin biopsy specimens of 13 revertant EB patients having correcting mutations in the COL17A1, LAMB3, or COL7A1 genes. Analysis revealed that lack of C17 led to decreased melanin intensity and melanocyte density in the epidermis when compared to the revertant patches. Reversions of LAMB3 and COL7A1 in keratinocytes did not influence clinical pigmentation or density of melanocytes. We conclude that in human skin, melanocyte supply to the epidermis depends on C17 expression in keratinocytes. This article is protected by copyright. All rights reserved.

PMID: 24330315 [PubMed – as supplied by publisher]

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Zinc gluconate is an agonist of peroxisome proliferator-activated receptor-α in the epidermis.

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Zinc gluconate is an agonist of peroxisome proliferator-activated receptor-α in the epidermis.

Exp Dermatol. 2012 May;21(5):347-51

Authors: Poiraud C, Quereux G, Knol AC, Allix R, Khammari A, Dreno B

Abstract
Peroxisome proliferator-activated receptors-α (PPARs-α) are nuclear receptors with anti-inflammatory properties. Zinc gluconate is efficient in the treatment of several inflammatory dermatoses. The aim of our work was to determine whether the modulation of PPAR-α expression and activity could be one of the mechanisms of action of zinc gluconate anti-inflammatory activity in inflammatory dermatoses. Thus, we used ex vivo skin explants incubated with lipopolysaccharide (LPS), a pro-inflammatory molecule, with or without zinc gluconate. We evaluated PPAR-α protein expression using immunohistochemistry, PPAR-α DNA-binding activity using an ELISA-like technique, and PPAR-α mRNA levels using quantitative PCR. On the one hand, we found that PPAR-α epidermal protein expression was stimulated by LPS and that LPS suppressed PPAR-α mRNA expression, without modifying its function. On the other hand, in inflammatory LPS-stimulated explants, zinc gluconate significantly upregulated PPAR-α function and mRNA expression level, without changing its epidermal protein expression. These results suggest that zinc gluconate may be a PPAR-α agonist, which might play a role in the anti-inflammatory activity of this molecule.

PMID: 22509831 [PubMed – indexed for MEDLINE]

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First symposium on natural gene therapy of the skin.

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First symposium on natural gene therapy of the skin.
Exp Dermatol. 2012 Mar;21(3):236-9
Authors: Pasmooij AM, Jonkman MF
PMID: 22379975 [PubMed – indexed for MEDLINE]

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High genetic diversity of Staphylococcus aureus strains colonizing patients with epidermolysis bullosa.

High genetic diversity of Staphylococcus aureus strains colonizing patients with epidermolysis bullosa.

Exp Dermatol. 2012 Jun;21(6):463-6

Authors: van der Kooi-Pol MM,…

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About the cutaneous targets of bexarotene in CTCL patients.

About the cutaneous targets of bexarotene in CTCL patients.
Exp Dermatol. 2010 Aug;19(8):e299-301
Authors: Knol AC, Quéreux G, Brocard A, Ballanger F, Khammari A, Nguyen JM, Dréno B
Abstract
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Absence of modulation of CD4+CD25 regulatory T cells in CTCL patients treated with bexarotene.

Absence of modulation of CD4+CD25 regulatory T cells in CTCL patients treated with bexarotene.
Exp Dermatol. 2010 Aug;19(8):e95-102
Authors: Knol AC, Quéreux G, Brocard A, Ballanger F, Khammari A, Nguyen JM, Dréno B
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Prognostic value of tumor-infiltrating Foxp3+ T-cell subpopulations in metastatic melanoma.

Prognostic value of tumor-infiltrating Foxp3+ T-cell subpopulations in metastatic melanoma.
Exp Dermatol. 2011 May;20(5):430-4
Authors: Knol AC, Nguyen JM, Quéreux G, Brocard A, Khammari A, Dréno B
Abstract
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Ex vivo demonstration of a synergistic effect of Adapalene and benzoyl peroxide on inflammatory acne lesions.

Ex vivo demonstration of a synergistic effect of Adapalene and benzoyl peroxide on inflammatory acne lesions.
Exp Dermatol. 2011 Oct;20(10):850-3
Authors: Zuliani T, Khammari A, Chaussy H, Knol AC, Dréno B
Abstract
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