Activated platelets trigger an inflammatory response and enhance migration of aortic smooth muscle cells.

Massberg, S; Vogt, F; Dickfeld, T; Brand, K; Page, S; Gawaz, M

2003

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Titel:: Activated platelets trigger an inflammatory response and enhance migration of aortic smooth muscle cells.
Dokumenttyp:: Journal Article; Article
Autor(en):: Massberg, S; Vogt, F; Dickfeld, T; Brand, K; Page, S; Gawaz, M
Abstract:: OBJECTIVE: Exposure of the subendothelium to flowing blood following rupture of atherosclerotic lesions or during balloon angioplasty initiates platelet adhesion to the vascular wall. Because activated platelets release proinflammatory mediators (e.g., interleukin (IL)-1beta) and secrete growth factors, platelet adhesion to the subendothelial matrix might contribute to the recruitment of inflammatory cells and promote migration and proliferation of vascular smooth muscle cells (SMCs). METHODS AND RESULTS: Here, we demonstrate that incubation of cultured monolayers of aortic SMCs with alpha-thrombin-activated platelets significantly enhances the secretion of monocyte chemoattractant protein-1 (MCP-1) (P<0.05) and promotes SMC migration (P<0.05). Platelet-induced secretion of MCP-1 was abolished by anti-IL-1alpha and beta monoclonal antibodies or the IL-1 receptor antagonist (IL-1RA). In contrast, platelet-mediated SMC migration was attenuated only by anti-platelet-derived growth factor (PDGF)-mAb but not by IL-1RA. Correspondingly, recombinant human interleukin-1 (rhIL-1) beta increased MCP release by SMCs but had no effect on SMC migration. Platelet-mediated MCP secretion by SMCs involved the activation and nuclear translocation of the transcription factor nuclear factor-kappaB (NF-kappaB). CONCLUSION: Therefore, platelet adhesion to the subendothelium increases the chemotactic and migratory properties of SMC and is likely to contribute substantially to the process of atherosclerosis and vessel (re-)stenosis.
Zeitschriftentitel:: Thromb Res
Jahr:: 2003
Band / Volume:: 110
Heft / Issue:: 4
Seitenangaben Beitrag:: 187-94
Sprache:: eng
PubMed:: http://view.ncbi.nlm.nih.gov/pubmed/14512080
Print-ISSN:: 0049-3848
TUM Einrichtung:: I. Medizinische Klinik und Poliklinik (Kardiologie); Institut für Klinische Chemie und Pathobiochemie
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mediaTUM Gesamtbestand Einrichtungen Schools TUM School of Medicine and Health Departments Clinical Medicine Klinik und Poliklinik für Innere Medizin I, Kardiologie (Prof. Laugwitz)2003

mediaTUM Gesamtbestand Einrichtungen Schools TUM School of Medicine and Health Departments Clinical Medicine Institut für Klinische Chemie und Pathobiochemie (Prof. Ruland)2003