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Biotech / Medical : Cistron Biotechnology(CIST)$.30 -- Ignore unavailable to you. Want to Upgrade?

To: Steve Harmon who wrote (1997)	3/7/1999 1:04:00 AM
From: Walter Morton	Read Replies (1) \| Respond to of 2742

Abstract Endothelium-derived relaxing factor is thought to produce and maintain vascular relaxation. Nitric oxide accounts for the biological activity of EDRF and is produced by the endothelial nitric oxide synthase. Chronic hypoxia and proinflammatory stimulators such as LPS (Lipopolysaccharides from Pseudomonas aeroginosa) and Il-1b (Interleukin-1b ) have been shown to produce pulmonary hypertension and to induce vascular remodeling of small pulmonary arteries in animal models (Rabinovitch, 1979 and Graham, 1990). The purpose of this study was to characterize the influence of these factors on the regulation of the endothelial nitric oxide synthase (eNOS) in human pulmonary artery endothelial cells (HPAEC). To adress this question I established a culture of HPAEC and exposed the cell lines to hypoxia (3% O2), Il-1b , TNFa and LPS either alone or to hypoxia in combination with Il-1b , TNFa or LPS. The mRNA and whole protein were extracted to the following time points: 24, 48 and 96 hours after begin of exposion. The eNOS mRNA and protein expression were analyzed using northern and western blotting techniques. Additionally, monitoring of the mRNA expression of the vasoconstructive and vasoproliferative mediators endothelin-1 (ET-1) and interleukin-8 (Il-8) were performed using northern blotting. The presented data show that hypoxia and proinflammatory stimulators as well as the combination of both induce a downregulation of the eNOS protein. The parallel downregulation of the eNOS mRNA strongly suggests that this regulation takes place at the transcriptional level. The same stimuli upregulate the ET-1 and Il-8 mRNA. These findings indicate that the reciprocal regulation of vasodilators and vasoconstrictors contribute to the pathomechanisms involved in the development of pulmonary hypertension. -------------------------------------------------------------------------------- © Die inhaltliche Zusammenstellung und Aufmachung dieser Publikation sowie die elektronische Verarbeitung sind urheberrechtlich geschützt. Jede Verwertung, die nicht ausdrücklich vom Urheberrechtsgesetz zugelassen ist, bedarf der vorherigen Zustimmung. Das gilt insbesondere für die Vervielfältigung, die Bearbeitung und Einspeicherung und Verarbeitung in elektronische Systeme.