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Effect of Growth Factors on Human Vascular Endothelial Cell Prostacyclin Production

Effect of Growth Factors on Human Vascular Endothelial Cell Prostacyclin Production Prostacyclin (PGIj) Is an anttthrombotic factor, which may prevent the initiation and the complications of arteriosclerosis. The most Important site of PGI2production Is the vascular endothellum, but little is known about how this process is regulated. In this connection, there Is special Interest In the roles of various growth factors released from platelets, macrophages, vascular smooth muscle cells, and the endothelial cells themselves. We investigated the effects of transforming growth factor-β (TGF-β), plateletderived growth factor (PDGF), and acidic and basic flbroblast growth factors (aFGF and bFGF) on the PGI2production of cultured human umbilical vein endothelial cells by measuring the stable metabolite of PGI2, 6-keto-prostaglandln F1a)by radlolmmunoassay. TGF-0 Induced doseand time-dependent stimulation of PGI2production. The lowest stimulatory concentration of TGF-β was 0.1 ng/ml, and the maximal response, a 2.1-fold rise, was obtained with 1.0 ng/ml. The effect of TGF-0 lasted 48 hours and was blocked by Inhibitors of transcription, translation, and cydooxygenase. Maximal stimulation by TGF-β was enhanced by epidermal growth factor. PDGF and bFGF had no effect on PGI2production, but aFGF Inhibited It This Is the first demonstration that TGF-0 enhances PGI2production by human vascular cells, and this phenomenon may be part of negative feedback mechanisms that prevent thrombosis and arteriosclerosis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Effect of Growth Factors on Human Vascular Endothelial Cell Prostacyclin Production

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Copyright
© 1990 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Prostacyclin (PGIj) Is an anttthrombotic factor, which may prevent the initiation and the complications of arteriosclerosis. The most Important site of PGI2production Is the vascular endothellum, but little is known about how this process is regulated. In this connection, there Is special Interest In the roles of various growth factors released from platelets, macrophages, vascular smooth muscle cells, and the endothelial cells themselves. We investigated the effects of transforming growth factor-β (TGF-β), plateletderived growth factor (PDGF), and acidic and basic flbroblast growth factors (aFGF and bFGF) on the PGI2production of cultured human umbilical vein endothelial cells by measuring the stable metabolite of PGI2, 6-keto-prostaglandln F1a)by radlolmmunoassay. TGF-0 Induced doseand time-dependent stimulation of PGI2production. The lowest stimulatory concentration of TGF-β was 0.1 ng/ml, and the maximal response, a 2.1-fold rise, was obtained with 1.0 ng/ml. The effect of TGF-0 lasted 48 hours and was blocked by Inhibitors of transcription, translation, and cydooxygenase. Maximal stimulation by TGF-β was enhanced by epidermal growth factor. PDGF and bFGF had no effect on PGI2production, but aFGF Inhibited It This Is the first demonstration that TGF-0 enhances PGI2production by human vascular cells, and this phenomenon may be part of negative feedback mechanisms that prevent thrombosis and arteriosclerosis.

Journal

ArteriosclerosisWolters Kluwer Health

Published: Jul 1, 1990

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