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Am J Physiol Lung Cell Mol Physiol (September 27, 2002). doi:10.1152/ajplung.00042.2002
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Articles in PresS, published online ahead of print September 27, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00042.2002
Submitted on January 28, 2002
Accepted on September 23, 2002

The effect of cigarette smoke on fibroblast-mediated gel contraction is dependent on cell density

Hangjun Wang1, Xiangde Liu2, Takeshi Umino3, Tadashi Kohyama4, Yun Kui Zhu5, Fu-Qiang Wen2, John R. Spurzem2, Debra J. Romberger2, Hui Jung Kim6, and Stephen I. Rennard2*

1 Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada
2 Department of Pulmonary & Critical Care Section, Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA
3 Department of Pulmonary Medicine, Tokyo Medical & Dental University, Tokyo, Japan
4 Department of Respiratory Medicine, University of Tokyo, Tokyo, Japan
5 Department of Respiratory Diseases, Jincheng Hospital, Lanzhou, China
6 Department of Internal Medicine, Seoul Adventist Hospital, Seoul, Korea, Republic of

* To whom correspondence should be addressed. E-mail: srennard{at}unmc.edu.

Cigarette smoke exposure has been associated with a variety of diseases, including emphysema. The current study evaluated the interaction of cell density and cigarette smoke extract (CSE) on fibroblast contraction of collagen gels. Protein levels of TGF-ß1, fibronectin and PGE2 and TGF-ß1 mRNA were quantified. Although both 5% and 10% CSE inhibited contraction by low-density fibroblasts (1x105 cell/ml), only 5% CSE augmented contraction in higher-density cultures (3-5 x105 cells/ml). CSE also inhibited fibronectin and TGF-ß1 production in low-density cultures, but stimulated fibronectin production in high-density cultures. Active TGF-ß1 was readily detectable only in higher-density cultures, and was markedly augmented by 5% CSE. In contrast, although TGF-ß1 mRNA expression was inhibited in high-density cultures by 10% CSE, expression was increased in the presence of 5% CSE. These results suggest that CSE-induced inhibition of low-density fibroblast contraction is due to inhibition of fibronectin production, while CSE's stimulatory effect on high-density cells is the result of increased release of TGF-ß1. These effects may help explain the varied pathologies associated with exposure to cigarette smoke.




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