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Am J Physiol Lung Cell Mol Physiol 281: L403-L411, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 2, L403-L411, August 2001

Cigarette smoke extract induces endothelin-1 via protein kinase C in pulmonary artery endothelial cells

Sang-Do Lee1, Dong-Soon Lee2, Yong-Gam Chun3, Tae-Sun Shim1, Chae-Man Lim1, Younsuck Koh1, Woo-Sung Kim1, Dong-Soon Kim1, and Won-Dong Kim1

1 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Asan Medical Center, College of Medicine Ulsan University, Songpa-gu, 138-736 Seoul; 2 Department of Clinical Pathology, Seoul National University Hospital, Chongro-gu, 110-744 Seoul; and 3 Asan Life Science Institute, 138-736 Seoul, Korea

We examined the mechanism of endothelin (ET)-1 regulation by cigarette smoke extract (CSE) and the effect of platelets on CSE-induced stimulation of ET-1 gene expression in human and bovine pulmonary artery endothelial cells (PAECs). Our data show that CSE (1%) induces ET-1 gene expression (after 1 h) and ET-1 peptide synthesis (after 4 h) in bovine PAECs. The induction of preproET-1 mRNA level was due to de novo transcription, and new protein synthesis was not required for this induction. The protein kinase C inhibitors staurosporine (10-8 mol/l) and calphostin C (10-7 mol/l) abolished the induction of ET-1 gene expression by CSE in bovine and human PAECs. Although a lower concentration of platelets (106 cells/ml in bovine PAECs; 107 cells/ml in human PAECs) did not significantly alter ET-1 gene expression in PAECs, incubation of platelets with CSE (1%) and PAECs produced a significant increase in preproET-1 mRNA and ET-1 peptide compared with the values in the presence of CSE (1%) alone. CSE (1%) induced platelet aggregation and increased the expression of platelet membrane glycoproteins ex vivo. Thus our data suggest that CSE stimulates ET-1 gene expression via PKC in PAECs. CSE and platelets showed a synergistic effect on ET-1 gene expression, possibly through the activation of platelets by CSE.

endothelium


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