Background: β 1-integrins, which localize to the basolateral surface of basal keratinocytes, are important in the differentiation control and proliferation of the epidermis. Many cutaneous diseases with perturbed dif...Background: β 1-integrins, which localize to the basolateral surface of basal keratinocytes, are important in the differentiation control and proliferation of the epidermis. Many cutaneous diseases with perturbed differentiation, including arsenical keratosis, show altered patterns of integrin distribution and expression. Arsenic may induce arsenical keratosis through the differentiation and apoptosis aberration by integrins. The purpose of this study is to investigate the role of integrin and arsenic in the pathogenesis of arsenical keratosis. Methods: Twenty-five specimens obtained from25 patients with arsenical keratosis disease were studied. Immunohistochemistry staining to β 1, α 2β 1, or α 3β 1 integrins was performed in arsenical keratosis and clinically normal perilesional skin. Western blotting was used to assess the expression of integrin β 1 and focal adhesion kinase (FAK) in arsenic-treated cultured keratinocytes. Results: A decreased expression of β 1, α 2β 1, or α 3β 1 integrins was demonstrated in arsenical keratosis and clinical normal perilesional skin in a large proportion of arsenical keratosis cases studied. The expressions of integrin β 1 and FAK were both decreased in arsenic-treated keratinocytes. Conclusions: Our results suggest that arsenic induces abnormal differentiation in arsenical keratosis via the effects of integrin expression in keratinocytes.展开更多
文摘Background: β 1-integrins, which localize to the basolateral surface of basal keratinocytes, are important in the differentiation control and proliferation of the epidermis. Many cutaneous diseases with perturbed differentiation, including arsenical keratosis, show altered patterns of integrin distribution and expression. Arsenic may induce arsenical keratosis through the differentiation and apoptosis aberration by integrins. The purpose of this study is to investigate the role of integrin and arsenic in the pathogenesis of arsenical keratosis. Methods: Twenty-five specimens obtained from25 patients with arsenical keratosis disease were studied. Immunohistochemistry staining to β 1, α 2β 1, or α 3β 1 integrins was performed in arsenical keratosis and clinically normal perilesional skin. Western blotting was used to assess the expression of integrin β 1 and focal adhesion kinase (FAK) in arsenic-treated cultured keratinocytes. Results: A decreased expression of β 1, α 2β 1, or α 3β 1 integrins was demonstrated in arsenical keratosis and clinical normal perilesional skin in a large proportion of arsenical keratosis cases studied. The expressions of integrin β 1 and FAK were both decreased in arsenic-treated keratinocytes. Conclusions: Our results suggest that arsenic induces abnormal differentiation in arsenical keratosis via the effects of integrin expression in keratinocytes.
