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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Thrombospondin-1 induces matrix metalloproteinase-2 activation in vascular smooth muscle cells.

INTRODUCTION: Thrombospondin-1 (TSP-1), an extracellular matrix (ECM) glycoprotein, is associated with a variety of cellular processes relevant to atherosclerosis and intimal hyperplasia, including vascular smooth muscle cell (VSMC) migration. Matrix metalloproteinase-2 (MMP2) is associated with basement membrane and ECM degradation, important processes for cell migration. We hypothesized that TSP-1 modulates MMP2 activity in VSMCs and is critical for VSMC migration. METHODS: Quiescent bovine aortic VSMCs (48 hours) were incubated in serum-free media (SFM) with or without TSP-1 (10 or 20 microg/mL). Gelatinase activity was measured with zymography to determine pro-MMP2 and MMP2 activity. MMP2 messenger RNA expression was determined with Northern blot analysis. Invasion assays were performed. A binding assay was used to determine the specificity of TSP-1 binding to MMP2. Blots were quantified with densitometry, and all comparisons were made with a paired t test. RESULTS: TSP-1 induced production of activated forms of MMP2, as well as upregulation of pro-MMP2. MMP2 mRNA was upregulated 1.7-fold by TSP-1 at 10 and 20 microg/mL. GM6001, an MMP inhibitor, inhibited VSMC migration across the matrix barrier, whereas migration that occurred in the absence of the matrix barrier was unaffected. With a binding assay, TSP-1 interacted physically with MMP2, and TSP-1- bound MMP2 showed the strongest binding activity in comparison with collagen I, fibronectin, and elastin. CONCLUSION: TSP-1 induced MMP2 activation through transcriptional and posttranslational mechanisms. These findings imply that MMP2 activation is relevant to the mechanism of TSP-1-induced VSMC migration.[1]


  1. Thrombospondin-1 induces matrix metalloproteinase-2 activation in vascular smooth muscle cells. Lee, T., Esemuede, N., Sumpio, B.E., Gahtan, V. J. Vasc. Surg. (2003) [Pubmed]
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