Published online before print September 15, 2005, doi: 10.1161/01.RES.0000186276.06104.04
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© 2005 American Heart Association, Inc.
UltraRapid Communication |
Exogenous High-Mobility Group Box 1 Protein Induces Myocardial Regeneration After Infarction via Enhanced Cardiac C-Kit+ Cell Proliferation and Differentiation
From the Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’Immacolata, Istituto di Ricovero e Cura a Carattere Scientifico (F.L., A.Z., O.L., M.C.C.), Rome, Italy; Laboratorio di Biologia Vascolare e Terapia Genica, Centro Cardiologico Fondazione Monzino, Istituto di Ricovero e Cura a Carattere Scientifico (A.G., A.Di.C., G.P.), Milan, Italy; Fondazione Santa Lucia (G.B., L.B.), Rome, Italy; Department of Molecular Biology and Functional Genomics, San Raffaele Research Institute (R.P., S.M.), Milan, Italy; Department of Medicine, New York Medical College (J.K., R.R., P.A.), Valhalla, New York; San Raffaele University (M.E.B.), Milan, Italy.
Correspondence to Maurizio C. Capogrossi, Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’Immacolata-IDI, Via dei Monti di Creta 104, 00167 Rome, Italy. E-mail capogrossi{at}idi.it
High-mobility group box 1 protein (HMGB1) is a chromatin protein that is released by inflammatory and necrotic cells. Extracellular HMGB1 signals tissue damage, stimulates the secretion of proinflammatory cytokines and chemokines, and modulates stem cell function. The present study examined exogenous HMGB1 effect on mouse left-ventricular function and myocyte regeneration after infarction. Myocardial infarction was induced in C57BL/6 mice by permanent coronary artery ligation. After 4 hours animals were reoperated and 200 ng of purified HMGB1 was administered in the peri-infarcted left ventricle. This intervention resulted in the formation of new myocytes within the infarcted portion of the wall. The regenerative process involved the proliferation and differentiation of endogenous cardiac c-kit+ progenitor cells. Circulating c-kit+ cells did not significantly contribute to HMGB1-mediated cardiac regeneration. Echocardiographic and hemodynamic parameters at 1, 2, and 4 weeks demonstrated a significant recovery of cardiac performance in HMGB1-treated mice. These effects were not observed in infarcted hearts treated either with the unrelated protein glutathione S-transferase or a truncated form of HMGB1. Thus, HMGB1 appears to be a potent inducer of myocardial regeneration following myocardial infarction.
Key Words: myocardial infarction • regeneration • stem cells • cytokines
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