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Am J Physiol Lung Cell Mol Physiol 274: L854-L863, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 5, L854-L863, May 1998

Thrombin regulation of endothelin-1 gene in isolated human pulmonary endothelial cells

Catherine L. Golden1, Harry S. Nick2, and Gary A. Visner1,3

Departments of 3 Pediatrics, 1 Biochemistry and Molecular Biology, and 2 Neuroscience, University of Florida, Gainesville, Florida 32610

Endothelin (ET)-1 is a potent vasoconstrictor elicited from endothelial cells in response to a variety of stimuli and an important mediator for a variety of vascular diseases including pulmonary hypertension. In this paper, we describe the molecular regulation of the ET-1 gene in response to a vasoactive mediator, thrombin, in human pulmonary endothelial cells. Thrombin induces preproET-1 mRNA through a transcriptionally dependent mechanism, with a peak induction after 1 h of exposure. Analysis of chromatin structure identified several DNase I-hypersensitive regions under both basal and thrombin-stimulated conditions that reside in the 5'-promoter region, indicating that the ET-1 promoter is a constitutive promoter. Deletion analysis was employed as a functional assay to identify regions of the ET-1 promoter that are important in transcriptional regulation. We found that sites between -141 and -378 bp are essential for basal activity and that those between -378 and -484 bp are essential for thrombin-stimulated activity. However, full expression under both conditions required an element(s) within -952 bp.

chromatin studies; deletion analysis; pulmonary vascular disease


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