San Gallicano Dermatologic Institute

Rome, Italy

San Gallicano Dermatologic Institute

Rome, Italy
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Farage M.A.,Procter and Gamble | Berardesca E.,San Gallicano Dermatologic Institute | Maibach H.,University of California at San Francisco
Contact Dermatitis | Year: 2010

Dermatological responses are affected by the menstrual cycle phase in female patients, an unsurprising observation as oestrogen and progesterone affect the skin and immunological function, with oestrogen suppression of cellular immunity in particular. Exacerbation of dermatological symptoms is typically observed in either the latter phase of the menstrual cycle or during menstruation. The allergic response is diminished in the ovulatory phase and heightened in the progestinic phase. Definitive conclusions with regard to the effect of reproductive hormones on skin disorders have been somewhat hampered by a body of research that has employed diverse research parameters, such as dosage, testing sites, concentration, vehicle of irritant delivery, and method of assessment, however, individual patient sensitivity varies widely. Standardization of measurement techniques is necessary to provide reproducible results as much as individual patient variation and technique will allow. © 2009 John Wiley & Sons A/S.

Bellei B.,San Gallicano Dermatologic Institute | Maresca V.,San Gallicano Dermatologic Institute | Flori E.,San Gallicano Dermatologic Institute | Pitisci A.,San Gallicano Dermatologic Institute | And 2 more authors.
Journal of Biological Chemistry | Year: 2010

The synthesis of melanin pigments, or melanogenesis, is regulated by the balance of a variety of signal transduction pathways. Among these pathways, p38 MAPK signaling was found to be involved in stress-induced melanogenesis and to be activated byα-melanocyte-stimulating hormone (α-MSH) and ultraviolet irradiation. Previous studies have shown that α-MSH-stimulated melanogenesis can be inhibited by blocking p38 MAPK activity with SB203580, a pyridinyl imidazole compound. Consistent with this, we observed that pyridinyl imidazoles (SB203580 and SB202190) inhibited both basal and α-MSH-induced melanogenesis in B16 melanoma cells. However, SB202474, which has no ability to inhibit p38 MAPK activity and is usually used as a negative control compound in p38 MAPK studies, also suppressed melanin synthesis induction. Furthermore, the independence of the p38 kinase pathway from the repression of melanogenesis by pyridinyl imidazole compounds was also confirmed by small interfering RNA experiments. Interfering with p38 MAPK expression surprisingly stimulated melanogenesis and tyrosinase family protein expression. Although the molecular mechanism(s) by which p38 promotes the degradation of melanogenic enzymes remain to be determined, the involvement of the ubiquitin-proteasome pathway was demonstrated by co-treatment with the proteasomespecific inhibitor MG132 and the relative decrease in the ubiquitination of tyrosinase in cells transfected with p38-specific small interfering RNA. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.

Zouboulis C.C.,Dessau Medical Center | Jourdan E.,Laboratoire Dermatologique Bioderma | Picardo M.,San Gallicano Dermatologic Institute
Journal of the European Academy of Dermatology and Venereology | Year: 2014

Hyperseborrhoea has been considered as a major aetiopathogenetic factor of acne. However, changes in sebaceous gland activity not only correlate with seborrhoea but also with alterations in sebum fatty acid composition. Current findings indicate that sebum lipid fractions with proinflammatory properties and inflammatory tissue cascades are associated in the process of the development of acne lesions. The oxidant/antioxidant ratio of the skin surface lipids and alterations of lipid composition are the main players in the induction of acne inflammation. Nutrition may influence the development of seborrhoea, the fractions of sebum lipids and acne. Acne is an inflammatory disease probably triggered, among others, by proinflammatory sebum lipid fractions. © 2013 European Academy of Dermatology and Venereology.

Picardo M.,San Gallicano Dermatologic Institute | Bastonini E.,San Gallicano Dermatologic Institute
Journal of Investigative Dermatology | Year: 2015

Debate over the pathogenesis of vitiligo is still ongoing among scientists, with several hypotheses currently under consideration. The study by Wagner et al. in this issue focuses on the role of E-cadherin-mediated cell adhesion in vitiliginous epidermis under oxidative and mechanical stress. Their work highlights how alterations in cell-cell adhesion across nonlesional melanocyte membranes in patients with vitiligo argue for primary intrinsic defects in the melanocytes. © 2015 The Society for Investigative Dermatology.

Dell'Anna M.L.,San Gallicano Dermatologic Institute | Cario-Andre M.,French Institute of Health and Medical Research | Bellei B.,San Gallicano Dermatologic Institute | Taieb A.,French Institute of Health and Medical Research | Picardo M.,San Gallicano Dermatologic Institute
Experimental Dermatology | Year: 2012

Understanding the cellular and molecular mechanisms leading to melanocyte loss in vitiligo is a mandatory step in improving the overall management of vitiligo patients. Until now, the study of vitiligo was characterised by a fragmented approach, and it is very hard to share and compare the data obtained by the different teams. The scenario mirrors the pathogenic puzzle, but it delays a true productive focus on the disease. The in vitro research is based on different models, ranging from monolayer cell culture of epidermal and dermal cells or 3D reconstructed skin to histological data, gene expression, computer simulation profile. For each model, several different (biochemical, phenotypic, immunological) aspects have been considered, increasing the mass of data difficult to be merged. Our purpose was to provide a practical synopsis of consolidated and advanced possibilities in the study of vitiligo, showing how data have been poorly shared until now. Following a short overview of the background of the disease, the approaches, ranging from basic cell biology to molecular and 'omics' studies, are summarised. New fluorescent probes and techniques open new possibilities for functional studies. Next, intracellular and superficial markers of the melanocytes, the main involved cells, are listed. Moving the focus from the epidermal level to the systemic and subcellular ones, this review aims to propose innovative multidisciplinary options for the vitiligo understanding. This paper focuses on the major practical and theoretical questions to be solved. It may be the basis for a more coordinated and productive approach to the biological question. © 2012 John Wiley & Sons A/S.

Di Carlo A.,San Gallicano Dermatologic Institute
Giornale Italiano di Dermatologia e Venereologia | Year: 2012

Urethral discharge (UD) in men is one of the most identifiable sexually transmitted infections (STI)-associated syndromes. UD performs very well, giving the possibility of an accurate diagnosis, a treatment at first encounter, a rapid cure with effective drugs, a modification of the risk behavior. Furthermore the patient is informed about the infectious nature of STDs, the transmission through sexual intercourse, the increased risks of infertility and other complications and, finally, the importance of completing treatment, even after improvement. Applying the syndromic approach to UD has resulted in effective case management of urethritis, as shown in different studies. Thus, there are numerous reasons why treatment of gonorrhea should include a regimen with complete in vivo activity against both N. gonorrhoeae and C. trachomatis.

Bellei B.,San Gallicano Dermatologic Institute | Pitisci A.,San Gallicano Dermatologic Institute | Izzo E.,San Gallicano Dermatologic Institute | Picardo M.,San Gallicano Dermatologic Institute
PLoS ONE | Year: 2012

While investigating the role of p38 MAPK in regulating melanogenesis, we found that pyridinyl imidazole inhibitors class compounds as well as the analog compound SB202474, which does not inhibit p38 MAPK, suppressed both α-MSH-induced melanogenesis and spontaneous melanin synthesis. In this study, we demonstrated that the inhibitory activity of the pyridinyl imidazoles correlates with inhibition of the canonical Wnt/β-catenin pathway activity. Imidazole-treated cells showed a reduction in the level of Tcf/Lef target genes involved in the β-catenin signaling network, including ubiquitous genes such as Axin2, Lef1, and Wisp1 as well as cell lineage-restricted genes such as microphthalmia-associated transcription factor and dopachrome tautomerase. Although over-expression of the Wnt signaling pathway effector β-catenin slightly restored the melanogenic program, the lack of complete reversion suggested that the imidazoles interfered with β-catenin-dependent transcriptional activity rather than with β-catenin expression. Accordingly, we did not observe any significant change in β-catenin protein expression. The independence of p38 MAPK activity from the repression of Wnt/β-catenin signaling pathway was confirmed by small interfering RNA knockdown of p38 MAPK expression, which by contrast, stimulated β-catenin-driven gene expression. Our data demonstrate that the small molecule pyridinyl imidazoles possess two distinct and opposite mechanisms that modulate β-catenin dependent transcription: a p38 inhibition-dependent effect that stimulates the Wnt pathway by increasing β-catenin protein expression and an off-target mechanism that inhibits the pathway by repressing β-catenin protein functionality. The p38-independent effect seems to be dominant and, at least in B16-F0 cells, results in a strong block of the Wnt/β-catenin signaling pathway. © 2012 Bellei et al.

Bellei B.,San Gallicano Dermatologic Institute | Pitisci A.,San Gallicano Dermatologic Institute | Catricala C.,San Gallicano Dermatologic Institute | Larue L.,French Institute of Health and Medical Research | Picardo M.,San Gallicano Dermatologic Institute
Pigment Cell and Melanoma Research | Year: 2011

Wnt/β-catenin signaling plays important roles in many developmental processes including neural crest-derived melanocyte development and migration. However, the effective contribution of Wnt/β-catenin pathway in melanogenesis in adult human melanocytes has not been fully elucidated. Here, we report that in melanoma cells and in normal human melanocytes, melanogenesis stimulation by α-melanocyte-stimulating hormone (α-MSH) induces phosphorylation of β-catenin-Ser675 and stabilization of β-catenin protein. Activation of protein kinase A by α-MSH attenuates glycogen synthase kinase-3β, which regulates ubiquitin-dependent degradation of β-catenin, suggesting a coordinated mechanism of β-catenin activity stimulation. Consistent with increased nuclear β-catenin, cyclic adenosine monophosphate (cAMP) elevation facilitates β-catenin-dependent transactivation of many Wnt target genes. Moreover, chromatin immunoprecipitation assays demonstrated an increased association of β-catenin with the proximal promoter of microphthalmia-associated transcription factor, the master regulator of pigmentation. These results demonstrate the existence of cross talk between the cAMP and Wnt pathways in melanocytes, suggesting that β-catenin could play a key role in the physiological regulation of epidermal melanogenesis. © 2011 John Wiley & Sons A/S.

Maresca V.,San Gallicano Dermatologic Institute | Flori E.,San Gallicano Dermatologic Institute | Picardo M.,San Gallicano Dermatologic Institute
Pigment Cell and Melanoma Research | Year: 2015

Cutaneous phototype is considered mainly related to cutaneous pigmentation and to the eumelanin/pheomelanin ratio, which is mostly genetically determined by the melanocortin 1 receptor (MC1R) polymorphisms. However, data in literature indicate that, in addition to stimulation of eumelanin synthesis, the MC1R signalling activates antioxidant, DNA repair and survival pathways. New emerging aspects regarding photoprotection and skin phototypes are going beyond those features connected to the melanin content in the skin. Important new findings link the MC1R to nuclear receptors activation, shedding light on new extra-melanogenic effects dependent on the α-melanocyte-stimulating hormone (α-MSH) activity and new ways through which such functions are modulated. These evidences indicate that several factors including melanin play a part in defining the basis for individual sun sensitivity, suggesting that the cutaneous phototype represents a 'biochemical fingerprint'. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Di Carlo A.,San Gallicano Dermatologic Institute
Thermology International | Year: 2011

"Thermal stimulation", a method for improved thermographic identification of skin malignancies, was developed in the 1980-ies. The principle of this method and typical findings in malignant melanoma are described. The mechanism of observed temperature changes and future applications of this technique are discussed.

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