P347	Hepatocyte growth factor mediates induction of PAI-1, Il-6 and Il-8 in human adipose tissue.
1G.Rega, 1Chr.Kaun, 1T.Weiss, 1S.Demyanets, 2M.Frey, 1G.Maurer, 3K.Huber, 1J.Wojta
1Department of Internal Medicine II, Medical University Vienna, Vienna, AT; 2Department of Surgery, Medical University Vienna, Vienna, AT; 33rd Department of Medicine, Wilhelminenspital, Vienna, AT.

Background: Obesity is associated with an increased risk of developing cardiovascular disease. The pro-atherogenic adipokines plasminogen activator inhibitor-1 (PAI-1), interleukin (Il)-8 and Il-6 are elevated in patients with obesity, insulin resistance and type 2 diabetes. On the other hand serum hepatocyte growth factor (HGF) levels are also elevated in patients with atherosclerosis and obesity. In this study we investigate whether HGF regulates the expression of PAI-1, Il-6 and Il-8 in human adipose tissue. Methods: Primary human preadipocytes were prepared from visceral and subcutaneous adipose tissue. Differentiation to adipocytes was induced by hormone-supplementation. Preadipocytes and adipocytes were treated with HGF for 48h. PAI-1, Il-6 and Il-8 antigen were quantified by ELISA, mRNA levels were determined by RealTimePCR. Results: HGF significantly up-regulates PAI-1 production in both preadipocytes and adipocytes up to 9-fold and 6-fold, Il-6 production up to 18-fold and 13-fold and Il-8 production up to 6-fold in both cell types. These results were confirmed on the level of mRNA expression. Conclusion: Our results demonstrate a significant upregulation of PAI-1, Il-6 and Il-8 expression in human preadiopcytes and adipocytes. Since elevated levels of HGF have been seen in obese subjects one might speculate that HGF could contribute to increased levels of the adipokines PAI-1, Il-6 and Il-8 also seen in these patients and could thus be indirectly involved in the development and progression of atherosclerosic lesions.

Copyright © 2005 S. Karger AG, Basel. Any further use of this abstract requires written permission from the publisher.