Protein Information

ID 353
Name integrin
Synonyms Alpha 11 precursor; HsT18964; ITGA11; Integrin; Integrin alpha 11; Integrin alpha 11 precursor; MSTP018; HsT18964s…

Compound Information

ID 1225
Name acrolein
CAS 2-propenal

Reference

PubMed Abstract RScore(About this table)
9575878 Carnevali S, Nakamura Y, Mio T, Liu X, Takigawa K, Romberger DJ, Spurzem JR, Rennard SI: Cigarette smoke extract inhibits fibroblast-mediated collagen gel contraction. Am J Physiol. 1998 Apr;274(4 Pt 1):L591-8.
Cigarette smoking, the major cause of pulmonary emphysema, is characterized by destruction of alveolar walls. Because tissue destruction represents a balance between injury and repair, we hypothesized that cigarette smoke exposure may contribute to the development of emphysema through the inhibition of tissue contraction during the repair process. To partially evaluate this hypothesis, we investigated the effects of cigarette smoke extract (CSE) on the ability of cultured fibroblasts to mediate collagen gel contraction in vitro: CSE inhibited fibroblast-mediated gel contraction in a concentration-dependent manner (P < 0.01). Production of prostaglandin E2, a known inhibitor of fibroblast contraction, was unchanged by CSE as was cell surface integrin expression. In contrast, fibronectin production by fibroblasts was inhibited (P < 0.01), and addition of exogenous fibronectin partially restored the contractile activity, thus suggesting at least one mechanism to explain inhibition of gel contraction by CSE. When CSE was treated to remove volatile components, it showed less inhibitory activity on fibroblast-mediated gel contraction. Therefore, we also examined the effects of acrolein and acetaldehyde, two volatile components of cigarette smoke. Inhibition of contraction was observed at 5 microM acrolein and at 0.5 mM acetaldehyde. In conclusion, cigarette smoke inhibited fibroblast-mediated gel contraction, and this inhibition was due, at least in part, to the volatile components of cigarette smoke and may be mediated, at least in part, by a decrease in fibroblast fibronectin production. By inhibition of repair, these smoke components may contribute to the development of pulmonary emphysema.
1(0,0,0,1)