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(Circulation Research. 2004;95:446.)
© 2004 American Heart Association, Inc.

Editorials

Cell–Matrix Signaling and Thrombospondin

Another Link to Myocardial Matrix Remodeling

Francis G. Spinale

From the Division of Cardiothoracic Surgery, Department of Surgery, Medical University of South Carolina and RHJ Department of Veterans Affairs Medical Center, Charleston, SC.

Correspondence to Francis G. Spinale, Cardiothoracic Surgery, Rm 625, Strom Thurmond Research Bldg, 770 MUSC Complex, Medical University of South Carolina, 114 Doughty St, Charleston, SC 29425. E-mail wilburnm@musc.edu

See related article, pages 515–522

Key Words: hypertrophy • extracellular matrix • thrombospondin • matrix metalloproteinase

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Thrombospondins (TSP) are a family of secreted glycoproteins that participate in cell-to-matrix communication through a number of different pathways.^1–8 Although TSP were first identified as a protein released by platelets after exposure to thrombin (hence the origin of the name of this family of proteins), it is now recognized that TSP are released by a number of cell types. TSP are secreted into the extracellular matrix (ECM) and interact with a number of important bioactive molecules, such as transforming growth factor-ß (TGF-ß) and platelet-derived growth factor (PDGF).^1,2,4,9,10 In general terms, TSP appear to modulate cell/matrix interactions through the coalescence of membrane proteins and signaling molecules at specific contact points on the cell surface.^1,2,5,6 These sites of TSP/protein interactions at the cell surface, which then induce intracellular signaling events, include the integrins as well as integrin-associated proteins such as CD36 and CD47. Although 5 members of the TSP family exist, the best-studied are TSP-1 and TSP-2. The biological properties of TSP-1 and TSP-2 appear to be similar in general terms, but there are structural differences in TSP-1 and TSP-2 that may impart some unique functions with respect to cell-matrix signaling.^11–14 In this issue, Schroen et al report a potential role of myocardial TSP-2 in the adaptive and maladaptive remodeling that occurs in left ventricular hypertrophy (LVH).¹⁵ To place the findings of this study in context with emerging studies regarding myocardial ECM remodeling and the progression to LV failure, a brief review of the biology of TSP with respect to matrix signaling . . . [Full Text of this Article]