The Effect of Nicotine on Elastin Gene Expression in Cultured Skin Fibroblasts.
- Author:
Jee Ook KIM
1
;
Young Wook RYOO
;
Kyu Suk LEE
Author Information
1. Department of Dermatology, College of Medicine, Keimyung University, Taegu, Korea.
- Publication Type:Original Article
- Keywords:
Elastin gene expression;
Nicotine
- MeSH:
Animals;
Blotting, Northern;
Cats;
Chloramphenicol O-Acetyltransferase;
Cytokines;
Depression;
Elastic Tissue;
Elastin*;
Extracellular Matrix;
Fibroblasts*;
Gene Expression*;
Humans;
Intercellular Signaling Peptides and Proteins;
Metabolism;
Microscopy, Confocal;
Nicotine*;
Periodontal Diseases;
Peripheral Vascular Diseases;
Pulmonary Fibrosis;
RNA, Messenger;
Skin*;
Smoke;
Smoking;
Tobacco
- From:Korean Journal of Dermatology
2001;39(5):529-535
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The elastic fibers are a major fibrillar component of the extracellular matrix of several organs, and their presence provides elastic properties to these tissues. A variety of cytokines, growth factors, and hormones have been shown to modulate elastin gene expression. So far most interest increased the effects of external environment on elastin metabolism in the skin. It has become generally accepted that cigarette smoking contributes to accelerated coronary and peripheral vascular disease, pulmonary fibrosis and periodontal disease. Nicotine is a major component of the particulate phase of tobacco smoke. OBJECTIVE: Only little is known about the molecular and cellular mechanism underlying the effect of nicotine on the skin fibroblasts. Our study was performed to determine the effects of nicotine on elastin gene expression. METHOD: In this study, the effects of nicotine were examined by Northern blot hybridization, chloramphenicol acetyltransferase (CAT) assay, and laser scanning microscopy in cultured human fibroblasts. RESULTS: In Northern blot hybridization, steady-state levels of elastin mRNA were decreased 0.9-fold at 1 microgram/mL of nicotine, 0.7-fold at 10 microgram/mL and 0.5-fold at 100 microgram/mL, compared to untreated control. Nicotine caused a marked alteration in the elastin mRNA expression in a dose-related fashion. In CAT assay, the relative elastin CAT activity was 1.0 in the untreated control, 0.9 at a concenturation of 1 microgram/mL, 0.3 at 10 microgram/mL, and 0.2 at 100 microgram/mL. Nicotine caused a marked decrease on elastin promoter activity. In laser scanning microscopy, the immunosignal for elastin in nicotine-treated fibroblasts shows in less intense than in untreated control. CONCLUSION: These results indicate that nicotine may be a powerful down-regulator of elastin production, suggesting transcriptional depression of gene expression in cultured skin fibroblasts.
