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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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1437-4315
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Volume 383, Issue 1

Issues

Monocyte-Expressed Urokinase Regulates Human Vascular Smooth Muscle Cell Migration in a Coculture Model

Angelika Kusch / Sergey Tkachuk / Steffen Lutter / Hermann Haller / Rainer Dietz / Martin Lipp / Inna Dumler
Published Online: 2005-06-01 | DOI: https://doi.org/10.1515/BC.2002.022

Abstract

Interactions of vascular smooth muscle cells (VSMC) with monocytes recruited to the arterial wall at a site of injury, with resultant modulation of VSMC growth and migration, are central to the development of vascular intimal thickening. Urokinasetype plasminogen activator (uPA) expressed by monocytes is a potent chemotactic factor for VSMC and might serve for the acceleration of vascular remodeling. In this report, we demonstrate that coculture of human VSMC with freshly isolated peripheral bloodderived human monocytes results in significant VSMC migration that increases during the coculture period. Accordingly, VSMC adhesion was inhibited with similar kinetics. VSMC proliferation, however, was not affected and remained at the same basal level during the whole period of coculture. The increase of VSMC migration in coculture was equivalent to the uPAinduced migration of monocultured VSMC and was blocked by addition into coculture of soluble uPAR (suPAR). Analysis of uPA and uPAR expression in cocultured cells demonstrated that monocytes are a major source of uPA, whose expression increases in coculture fivefold, whereas VSMC display an increased expression of cell surfaceassociated uPAR. These findings indicate that upregulated uPA production by monocytes following vascular injury acts most likely as an endogenous activator of VSMC migration contributing to the remodeling of vessel walls.

About the article

Published Online: 2005-06-01

Published in Print: 2002-01-23


Citation Information: Biological Chemistry, Volume 383, Issue 1, Pages 217–221, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2002.022.

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