A Role of Plasminogen in Atherosclerosis and Restenosis Models in Mice

Edward F. Plow; Victoria A. Ploplis; Steven Busuttil; Peter Carmeliet; Desire Collen

doi:10.1055/s-0037-1615544

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1999; 82(S 01): 4-7
DOI: 10.1055/s-0037-1615544

Commentaries

Schattauer GmbH

A Role of Plasminogen in Atherosclerosis and Restenosis Models in Mice

Edward F. Plow

¹From the Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Cleveland Clinic Foundation, Cleveland, OH

,

Victoria A. Ploplis

²W. M. Keck Transgene Center, Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN

,

Steven Busuttil

³Cleveland Veterans Administration Medical Center, Section of Vascular Surgery, Cleveland, OH, USA

,

Peter Carmeliet

⁴Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute of Biotechnology, University of Leuven, Leuven, Belgium

,

Desire Collen

⁴Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute of Biotechnology, University of Leuven, Leuven, Belgium

› Institutsangaben

Abstract

Summary

In addition to its preeminent role in fibrinolysis, the plasminogen system is believed to play a key role in mediating cell migration. Leukocyte migration into the vessel wall is a key and early event in the development of the lesions of atherosclerosis and restenosis, pathologies which may be viewed as specific examples of vascular inflammatory responses. The development of mice in which the plasminogen gene has been inactivated affords an opportunity to test the contribution of plasminogen in leukocyte migration during in vivo. This article summarizes recent studies conducted in murine models of the inflammatory repsonse, restenosis and atherosclerosis in which leukocyte migration, and in particular monocyte/macrophage migration, has been evaluated in plasminogen-deficient mice. Recruitment of these cells through the vessel wall in inflammatory response models and into the vessel wall in restenosis and transplant atherosclerosis models is substantially blunted. These data implicate plasminogen in the migration of leukocytes in these murine models. With the numerous correlations between components and/or activation of the plasminogen system in restenosis and atherosclerosis, these results also support a role of plasminogen in the corresponding human pathologies.

Key words

Leukocytes - macrophages - smooth muscle cells - inflammation

Volltext

Referenzen

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