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Background: Psoriasis is characterized by aberrant activation of several pro‐inflammatory circuits as well as abnormal hyperproliferation and dysregulated apoptosis of keratinocytes (KCs). Most currently available therapeutic options primarily target psoriasis‐associated immunological defects rather than epidermal abnormalities. Objective: To investigate the efficacy of the histone deacetylase (HDAC) inhibitor, Vorinostat, in targeting hyperproliferation and impaired apoptosis in psoriatic skin. Methods: Vorinostat effect was investigated in primary KCs cell cultures using cell cycle analysis by flow cytometry, apoptosis assays (Annexin V‐FICH and caspase‐3/7) and antibody arrays, qRT‐PCR and immunohistochemistry. Vorinostat impact on clinical manifestations of psoriasis was investigated in a chimeric mouse model. Results: Vorinostat was found to inhibit KCs proliferation and to induce their differentiation and apoptosis. Using a chimeric mouse model, vorinostat was found to result in marked attenuation of a psoriasiform phenotype with a significant decrease in epidermal thickness and inhibition of epidermal proliferation. Conclusions: Our results support the notion that vorinostat, a prototypic HDAC inhibitor, may be of potential use in the treatment of psoriasis and other hyperproliferative skin disorders. [ABSTRACT FROM AUTHOR]

Many lessons in autoimmunity--particularly relating to the role of immune privilege and the interplay between genetics and neuroimmunology--can be learned from the study of alopecia areata, the most common cause [...]

Abstract Adipose tissue injection as a free graft for the correction of soft tissue defects is a widespread procedure in plastic surgery. The main problem in achieving long-term soft tissue [...]

Abstract The injection of autologous free fat obtained by suction-assisted lipectomy for the correction of soft tissue defects is a common procedure in plastic surgery. However, unpredictable partial absorption of [...]

The goal of this study was to determine the role of Fas-mediated apoptosis in human epidermal aging. Epidermal Fas expression and apoptosis are increased in aged human skin. Aging changes of human epidermis, including decreased epidermal thickness and proliferation, are reversed following grafting of human skin to SCID (severe combined immunodeficiency) mice. Skin from aged participants (n = 14; mean 70.7 years), and young participants (n = 14; mean 23.4 years) was grafted to beige SCID mice, and epidermal thickness, proliferation (Ki-67 expression), apoptosis (TUNEL [Tdt-mediated dUTP nick end labeling] reaction below granular layer), and expression of Fas and FasL were determined by histology and immunochemical staining. Aged skin was associated with thinning of the epidermis, decreased epidermal proliferation, a significant increase in apoptosis below the granular layer, and epidermal Fas expression. Engraftment significantly reversed these aging changes, including apoptosis, and Fas expression. Correlation of reversal of aging changes, with decreased epidermal Fas expression and apoptosis, supports a role for Fas-mediated apoptosis in aging of human epidermis.

It has long been known that there is a special affinity of psoriasis for the scalp: Here, it occurs most frequently, lesions terminate sharply in frontal skin beyond the hair line and are difficult to treat. Yet, surprisingly, scalp psoriasis only rarely causes alopecia, even though the pilosebaceous unit clearly is affected. Here, we systematically explore the peculiar, insufficiently investigated connection between psoriasis and growing (anagen) terminal scalp hair follicles (HFs), with emphasis on shared regulatory mechanism and therapeutic targets. Interestingly, several drugs and stressors that can trigger/aggravate psoriasis can inhibit hair growth (e.g. beta‐blockers, chloroquine, carbamazepine, interferon‐alpha, perceived stress). Instead, several anti‐psoriatic agents can stimulate hair growth (e.g. cyclosporine, glucocorticoids, dithranol, UV irradiation), while skin/HF trauma (Köbner phenomenon/depilation) favours the development of psoriatic lesions and induces anagen in "quiescent" (telogen) HFs. On this basis, we propose two interconnected working models: (a) the existence of a bidirectional "hair follicle‐psoriasis axis," along which keratinocytes of anagen scalp HFs secrete signals that favour the development and maintenance of psoriatic scalp lesions and respond to signals from these lesions, and (b) that anagen induction and psoriatic lesions share molecular "switch‐on" mechanisms, which invite pharmacological targeting, once identified. Therefore, we advocate a novel, cross‐fertilizing and integrative approach to psoriasis and hair research that systematically characterizes the "HF‐psoriasis axis," focused on identification and therapeutic targeting of selected, shared signalling pathways in the future management of both, psoriasis and hair growth disorders. [ABSTRACT FROM AUTHOR]