AJP - Heart AJP citation statistics
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 279: H2865-H2871, 2000;
0363-6135/00 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (11)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Haug, C.
Right arrow Articles by Rozdzinski, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Haug, C.
Right arrow Articles by Rozdzinski, E.
Vol. 279, Issue 6, H2865-H2871, December 2000

Hepatocyte growth factor is upregulated by low-density lipoproteins and inhibits endothelin-1 release

Cornelia Haug1, Alexandra Schmid-Kotsas1, Ulrike Zorn1, Max G. Bachem1, Sabine Schuett1, Adolf Gruenert1, and Eva Rozdzinski2

1 Institute of Clinical Chemistry and 2 Department of Microbiology, University Hospital Ulm, D-89070 Ulm, Germany

Low-density lipoproteins (LDL) are known to cause endothelial injury and to promote the development of atherosclerotic lesions. This study demonstrates a significant concentration-dependent stimulatory effect of LDL on hepatocyte growth factor (HGF) synthesis (maximum release: 423 ± 16% of control) and HGF receptor mRNA expression in cultured human coronary artery endothelial cells (HCAEC). HGF is a potent mitogen for endothelial cells but does not affect smooth muscle cell proliferation. In contrast, endothelin-1 (ET-1) acts as a mitogen on vascular smooth muscle cells and seems to be upregulated in coronary atherosclerosis. In this study, the basal ET-1 synthesis in HCAEC was concentration-dependently reduced by HGF (minimum: 54 ± 3% of control). This inhibitory effect seems to be mediated via the tyrosine kinase activity of the HGF receptor c-met, since it was antagonized by the tyrosine kinase inhibitor lavendustin A. In addition, HGF also significantly reduced the LDL-stimulated ET-1 release. The LDL-induced upregulation of HGF synthesis in HCAEC and the inhibitory effect of HGF on ET-1 synthesis suggest a protective role of HGF in coronary atherosclerosis.

endothelin; endothelial cells


This article has been cited by other articles:


Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
D. X.-F. Deng, J. M. Spin, A. Tsalenko, A. Vailaya, A. Ben-Dor, Z. Yakhini, P. Tsao, L. Bruhn, and T. Quertermous
Molecular Signatures Determining Coronary Artery and Saphenous Vein Smooth Muscle Cell Phenotypes: Distinct Responses to Stimuli
Arterioscler Thromb Vasc Biol, May 1, 2006; 26(5): 1058 - 1065.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
P. Biswas, A. Roy, R. Gong, A. Yango, E. Tolbert, J. Centracchio, and L. D. Dworkin
Hepatocyte growth factor induces an endothelin-mediated decline in glomerular filtration rate
Am J Physiol Renal Physiol, January 1, 2005; 288(1): F8 - F15.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online