Immunolocalization of MUC1 in chronic plaque psoriasis.

Psoriasis is a chronic skin inflammatory disease with immunological, hyperproliferative and angiogenic dysfunction. MUC1 is a molecular sensor and signal transductor that responds to external stimuli generating cellular responses, which include cell proliferation, growth, differentiation, migration, invasion, survival and secretion of growth factors, and cytokines. The current study aimed at evaluation of the possible role of MUC1 in the pathogenesis of psoriasis through its immunohistochemical localization in involved and uninvolved psoriatic skin compared to normal skin in addition of correlating MUC1 expression with the clinical and pathological parameters of psoriasis. The current study investigated 30 patients with psoriasis and 10 controls. MUC1 was expressed in epidermis in 30% of normal skin compared to 20% of uninvolved epidermis and 63.3% of involved epidermis of psoriatic skin. MUC1 was seen staining endothelial cells of capillaries and inflammatory cells in dermis in 10% of normal skin, 0% of uninvolved psoriasis, and 83.3% of involved psoriasis. Dermal expression of MUC1 in psoriasis was associated with mild to moderate degrees of epidermal acanthosis (p = .027). Intense MUC1 expression by psoriatic epidermis was associated with short disease duration (p = .044). The upregulation of MUC1 in involved psoriatic lesion compared to uninvolved and normal skin may suggest MUC1 role in pathogenesis of psoriasis especially early stages. MUC1 may be responsible for less severity of psoriasis in old aged patients.

Immunohistochemical expression HIF1α in chronic plaque psoriasis, an association with angiogenesis and proliferation.

Psoriasis is characterized by excessive cell proliferation, angiogenesis, and regions of hypoxia. Hypoxia stimulates production of hypoxia inducible factors (HIFs) such as HIF1α. The aim of the present study is to investigate the possible role of HIF1α in pathogenesis of psoriasis and to correlate its expression with angiogenesis and proliferation in involved and uninvolved skin in patients with plaque psoriasis using CD34 and Ki-67. The current study was performed on 40 skin specimens of patients presented with chronic plaque psoriasis both involved and uninvolved together with 40 specimens from age- and sex-matched healthy volunteers as a control group. The specimens were submitted for HIF1α, CD34, and Ki-67 immunostaining. HIF1α was expressed in 37.5% of normal skin with mild intensity and cytoplasmic localization instead of its expression in 72.5% and 100% of uninvolved and involved psoriatic skin, respectively. Nucleocytoplasmic pattern of HIF1α was seen in 34.5% and 37.5% of uninvolved and involved psoriatic skin, respectively. Positive and intense expression of HIF1α as well as its nucleocytoplasmic localization were significantly in favor of psoriatic skin either involved or uninvolved in comparison to normal skin (P < 0.05). Intense HIF1α was significantly associated with microvessel density in both involved and uninvolved skin (P < 0.05). Nucleocytoplasmic pattern was significantly associated with epidermal acanthosis (P < 0.05) and tended to be associated with percentage of Ki-67 of psoriatic skin (P = 0.06). The present study demonstrated that HIF1α is upregulated in the skin of psoriatic cases (involved and uninvolved) compared to normal skin indicating its role in pathogenesis of psoriasis especially its active nuclear form that showed an association with angiogenesis and proliferation.