Related Experiment Video
Updated: Aug 13, 2026
In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration
Published on: February 23, 2019
Defective beta1-integrins expression in arsenical keratosis and arsenic-treated cultured human keratinocytes
Chih-Hung Lee1, Jau-Shiuh Chen, Yu-Lan Sun
1Department of Dermatology, Kaohsiung Medical University, Kaohsiung, Taiwan.
Background:
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.
Methods:
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.
Results:
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.
Conclusions:
Our results suggest that arsenic induces abnormal differentiation in arsenical keratosis via the effects of integrin expression in keratinocytes.
