[show abstract][hide abstract] ABSTRACT: Background and Objective. Suppression of apoptosis has been proposed as a mechanism responsible for epidermal thickness in psoriasis. Survivin is a member of the inhibitor of apoptosis family. Nuclear factor kappa B (NF-κB) is one of the transcriptional factors that regulate many genes affecting apoptosis. The aim of this study was to determine survivin and NF-κB expressions in psoriasis in comparison with normal epidermis. Patients and Methods. Immunohistochemical expressions of survivin and NF-κB were investigated in 41 psoriatic and 21 normal skin samples. Results. Diffuse nuclear survivin expression in all epidermal layers was seen in all of the psoriatic samples. NF-κB expression in different epidermal locations was seen in all of the psoriatic samples. Nuclear staining was positive in 40 psoriasis samples. Similar survivin and NF-κB expressions were observed in normal skin samples. Conclusion. Since similar expressions are seen in both normal and psoriatic epidermis, no important roles for survivin and NF-κB can be attributed in epidermal proliferation and thickness seen in psoriasis.
[show abstract][hide abstract] ABSTRACT: Survivin belongs to the inhibitor of apoptosis (IAP) protein family, and, in addition to the antiapoptotic functions, it also regulates the cell cycle. The survivin gene generates five major isoforms with diverse and opposite functions. Survivin is highly expressed in cancer and in few normal adult tissues, including skin. It is mostly detected in the nucleus of keratinocyte stem cells (KSCs), but it is also expressed in melanocytes and fibroblasts. Survivin isoforms are differentially detected in subpopulations of human keratinocytes, exerting contrasting activities. Survivin has an important role in the regulation of cell cycle in keratinocytes, and it protects these cells from anoikis and UV-induced apoptosis. In melanoma, survivin is abundantly expressed, and its subcellular localization varies depending upon tumor thickness and invasiveness. Survivin overexpression has been shown in squamous cell carcinoma (SCC), and it is also involved in UVB-induced carcinogenesis. The presence of survivin both in the nucleus and in the cytoplasm throughout the epidermal layers of psoriatic lesions suggests the involvement of this protein in the keratinocyte alterations typical of this disease. Additional studies on the expression of survivin isoforms and their subcellular localization in relation to function will confirm the key role of survivin in the skin and will open the field to new therapeutic strategies for many cutaneous conditions.
Journal of Investigative Dermatology 09/2011; 132(1):18-27. · 6.19 Impact Factor
[show abstract][hide abstract] ABSTRACT: Over the last two decades, research developments have revolutionized our understanding of the pathogenesis of psoriasis and of the contribution of several cytokines in the manifestation of the disease. The key role of TNF-α in the pathogenesis of psoriasis has been extensively studied and its therapeutic action, initially observed in experimental models, has been clinically translated into therapeutic agents with remarkable efficacy in the treatment of the disease. There are currently two classes of marketed biologic drugs that reduce TNF-α bioavailability and are used clinically in psoriasis: the soluble TNF-α receptor-Fc fusion protein (etanercept) and the anti-TNF-α monoclonal antibodies (adalimumab and infliximab). The present article reviews the pharmacodynamic properties of the three TNF-α inhibitors and discusses possible differences in their mode of action, clinical efficacy and safety profile.
Expert Review of Clinical Pharmacology 07/2011; 4(4):515-23.
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