الفهرس 
? Cell CycleOnly 14 pages are availabe for public view
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Abstract
Psoriasis vulgaris is a common skin disorder characterized by focal formation of inflamed, plaques that constantly shed scales derived from excessive growth of skin epithelial cells. The disease is defined by a series of linked cellular changes in the skin: hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils, and other types of leucocytes in affected skin. The cell cycle is an ordered set of events, culminating in cell growth and division into two daughter cells. The stages of cell cycle include; G1 stage which is the post-mitotic growth phase, the S stage which is the stage when DNA replication occurs, the G2 stage which is the pre-mitotic stage, and the M stage for mitosis. Cell-cycle progression is normally regulated by cyclins and cyclin inhibiting proteins. Progression of cells from G 1 to S phase is regulated via pRb phosphorylation by cyclin D complexed with CDK 4 and 6, which are in turn regulated by CDKI, such as p16 INK4 protein. It was reported that the proliferate cell population is approximately doubled in psoriasis, whereas the cell cycle is more than 8 times shorter (36 versus 311 hours) and daily production of keratinocytes in psoriatic lesions is approximately 28 times greater than that in normal epidermis. These observations encouraged us to investigate the expression of cyclin D1, as a positive regulator for cell cycle, in lesional psoriatic skin before and after receiving phototherapy and in normal skin in order to detect a possible role of it in the pathogenesis of psoriasis. The study was carried on thirty patients of psoriasis and ten controls of healthy individuals. Patients were either new cases that had not received any treatment yet or recurrent cases who were treated before by topical or systemic treatment. In these recurrent cases, the last treatment stopped two months before starting the phototherapy. Female patients who proved to be pregnant were excluded from the study. Skin biopsies were taken from affected skin of each patient before starting and after twenty four sessions of phototherapy and from controls to detect cyclin D1 in them. Statistical analysis of the results revealed the following: •Value of cyclin D1 expression in patients before phototherapy was significantly higher than that of controls. •Value of cyclin D1 in patients after 24 sessions of phototherapy was significantly decreased than that before phototherapy. •There was no statistically significant difference in the intensity of cyclin D1 between patients who were treated with UVB (narrow band) and those who were treated with PUVA. •There was no statistically significant correlation between both cyclin D1 in patients before therapy and the PASI score. •There was no statistically significant correlation between both cyclin D1 in patients before therapy and the duration of the disease. These findings indicate that cyclin D1 is significantly upregulated in psoriasis and thus it could play a role in the pathogenesis of psoriasis among other factors. In addition the significant change in the expression and intensity of cyclin D1 after phototherapy points that decrease of cyclin D1 could be one of the mechanisms by which UVR treats psoriasis.