Ann Dermatol.  2001 Sep;13(3):153-157. 10.5021/ad.2001.13.3.153.

Nicotine Down-regulates COL1A2 Promoter in Cultured Human Skin Fibroblasts


It has become generally accepted that cigarette smoking contributes to accelerated coronary and peripheral vascular disease, pulmonary fibrosis and periodontal disease. Moreover, it has been postulated that cigarette smoking causes skin-aging. Many of cutaneous manifestations of nicotine which is a major component of the particulate phase of tobacco smoke are related to its vasoconstrictive and thrombotic effects on the peripheral vascular system. How-ever, direct effect of nicotine on extracellular matrix (ECM) proteins including collagens is not well established. OBJECTIVE: To evaluate the effect of nicotine on type I collagen gene expression in cultured human skin fibroblasts.
After exposure to different doses of nicotine on cultured human skin fibroblasts, we examined the expressions of α1(I) procollagen gene and fibronectin gene by Northern blot analysis and chloramphenicol acetyltransferase (CAT) assay with CAT construct containing the 3.5 kb COL1A2 promoter.
In Northern blot hybridization, steady-state levels of α1(I) procollagen mRNA were decreased 0.8-fold at 1 µg/mL of nicotine, 0.5-fold at 10 µg/mL and 0.2-fold at 100 µg/mL, compared to untreated control. Those of fibronectin mRNA were decreased 0.9-fold, 0.7-fold, and 0.3-fold, respectively. In CAT assay, the relative COL1A2 CAT activity was 1.0 in the untreated control, 0.7 at a concentration of 1 µg/mL of nicotine, 0.5 at 10 µg/mL, and 0.3 at 100 µg/mL.
These results indicate that nicotine is a down-regulator of collagen gene expression at transcriptional level in vitro. We speculate that nicotine may contribute to the skin-aging by modulation of extracellular matrix gene expression including collagen as well as by its vasoconstrictive and thrombotic effects.


Nicotine; Collagen; In vitro
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