Lee Chih-Hung, Chen Jau-Shiuh, Sun Yu-Lan, Liao Wei-Ting, Zheng Ya-Wen, Chai Chih-Zin, Chen Gwo-Shing, Yu Hsin-Su
Department of Dermatology, Kaohsiung Medical University, Kaohsiung, Taiwan.
J Cutan Pathol. 2006 Feb;33(2):129-38. doi: 10.1111/j.0303-6987.2006.00361.x.
beta1-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.
Twenty-five specimens obtained from 25 patients with arsenical keratosis disease were studied. Immunohistochemistry staining to beta1, alpha2beta1, or alpha3beta1 integrins was performed in arsenical keratosis and clinically normal perilesional skin. Western blotting was used to assess the expression of integrin beta1 and focal adhesion kinase (FAK) in arsenic-treated cultured keratinocytes.
A decreased expression of beta1, alpha2beta1, or alpha3beta1 integrins was demonstrated in arsenical keratosis and clinical normal perilesional skin in a large proportion of arsenical keratosis cases studied. The expressions of integrin beta1 and FAK were both decreased in arsenic-treated keratinocytes.
Our results suggest that arsenic induces abnormal differentiation in arsenical keratosis via the effects of integrin expression in keratinocytes.
β1整合素定位于基底角质形成细胞的基底外侧表面，在表皮的分化控制和增殖中起重要作用。许多伴有分化紊乱的皮肤病，包括砷角化病，都显示出整合素分布和表达模式的改变。砷可能通过整合素导致的分化和凋亡异常诱导砷角化病。本研究的目的是探讨整合素和砷在砷角化病发病机制中的作用。
研究了从25例砷角化病患者获取的25个标本。对砷角化病组织及临床正常的病变周围皮肤进行β1、α2β1或α3β1整合素的免疫组织化学染色。采用蛋白质印迹法评估经砷处理的培养角质形成细胞中整合素β1和黏着斑激酶（FAK）的表达。
在所研究的大部分砷角化病病例中，砷角化病组织及临床正常的病变周围皮肤中β1、α2β1或α3β1整合素的表达均降低。经砷处理的角质形成细胞中整合素β1和FAK的表达均降低。
我们的结果表明，砷通过影响角质形成细胞中整合素的表达，在砷角化病中诱导异常分化。
