Profiling of gene expression using microarray in acrolein-treated human pulmonary fibroblasts

Abstract

Pulmonary fibroblasts are essential for the integrity of alveolar structures and to restore lung tissue after injury. They are also important for inflammatory responses through their ability to attract leukocytes. Cigarette smoke has many harmful components, and causes various pulmonary and lung diseases including chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema. Acrolein (ACR), one of the compounds in cigarette smoke, induces inflammatory cytokines and the generation of DNA adducts, resulting in dysfunction of respiratory cells such as pulmonary fibroblasts. In this study, we examined the expression of genes in ACR-treated human pulmonary fibroblasts by microarray profiling. We identified 2,378 and 312 genes that were differentially expressed within 6 h of treatment with 10 μM or 25 μM ACR, respectively. These genes were classified as being involved in many biological processes including apoptosis, immune responses, cell cycle, and signal transduction. Some genes, including HSPA1B, HMOX1, CASP3, PRDX3, and ANXA1, are related to COPD. These results support the hypothesis that ACR may increase cytotoxicity and tissue injury in respiratory cells and may attribute to the development of pulmonary disease.