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Am J Physiol Heart Circ Physiol 290: H232-H239, 2006. First published August 26, 2005; doi:10.1152/ajpheart.00457.2005
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Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction

Merry L. Lindsey,1 G. Patricia Escobar,1 Lawrence W. Dobrucki,2 Danielle K. Goshorn,1 Shenikqua Bouges,1 Joseph T. Mingoia,1 David M. McClister, Jr.,1 Haili Su,2 Joseph Gannon,3 Catherine MacGillivray,3 Richard T. Lee,3 Albert J. Sinusas,2 and Francis G. Spinale1,4

1Division of Cardiothoracic Surgery Research, Medical University of South Carolina, Charleston, South Carolina; 2Division of Cardiovascular Medicine, Department of Internal Medicine and Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, Connecticut; 3Cardiovascular Division, Department of Medicine Brigham and Women's Hospital and Harvard Medical School, Cambridge, Massachusetts; and 4Ralph A. Johnson Veterans Administration Medical Center, Charleston, South Carolina

Submitted 6 May 2005 ; accepted in final form 19 August 2005

Matrix metalloproteinases (MMPs) are postulated to be necessary for neovascularization during wound healing. MMP-9 deletion alters remodeling postmyocardial infarction (post-MI), but whether and to what degree MMP-9 affects neovascularization post-MI is unknown. Neovascularization was evaluated in wild-type (WT; n = 63) and MMP-9 null (n = 55) mice at 7-days post-MI. Despite similar infarct sizes, MMP-9 deletion improved left ventricular function as evaluated by hemodynamic analysis. Blood vessel quantity and quality were evaluated by three independent studies. First, vessel density was increased in the infarct of MMP-9 null mice compared with WT, as quantified by Griffonia (Bandeiraea) simplicifolia lectin I (GSL-I) immunohistochemistry. Second, preexisting vessels, stained in vivo with FITC-labeled GSL-I pre-MI, were present in the viable but not MI region. Third, a technetium-99m-labeled peptide (NC100692), which selectively binds to activated {alpha}v{beta}3-integrin in angiogenic vessels, was injected into post-MI mice. Relative NC100692 activity in myocardial segments with diminished perfusion (0–40% nonischemic) was higher in MMP-9 null than in WT mice (383 ± 162% vs. 250 ± 118%, respectively; P = 0.002). The unique finding of this study was that MMP-9 deletion stimulated, rather than impaired, neovascularization in remodeling myocardium. Thus targeted strategies to inhibit MMP-9 early post-MI will likely not impair the angiogenic response.

leukocytes; remodeling; imaging


Address for reprint requests and other correspondence: M. L. Lindsey, Cardiothoracic Surgery, Rm. 629, Strom Thurmond Research Bldg., 770 MUSC Complex, Medical Univ. of South Carolina, 114 Doughty St., PO Box 250778, Charleston, SC 29425 (e-mail: lindseym{at}uthscsa.edu)




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