hmgb1 attenuates cardiac remodelling in the failing heart via enhanced cardiac regeneration and mir-206-mediated inhibition of timp-3hmgb1减弱心脏重塑通过增强心脏衰竭的心脏再生和mir - 206抑制timp-3介导的.pdfVIP

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hmgb1 attenuates cardiac remodelling in the failing heart via enhanced cardiac regeneration and mir-206-mediated inhibition of timp-3hmgb1减弱心脏重塑通过增强心脏衰竭的心脏再生和mir - 206抑制timp-3介导的.pdf

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hmgb1 attenuates cardiac remodelling in the failing heart via enhanced cardiac regeneration and mir-206-mediated inhibition of timp-3hmgb1减弱心脏重塑通过增强心脏衰竭的心脏再生和mir - 206抑制timp-3介导的

HMGB1 Attenuates Cardiac Remodelling in the Failing Heart via Enhanced Cardiac Regeneration and miR-206- Mediated Inhibition of TIMP-3 1. 2. 2 2 3 Federica Limana , Grazia Esposito , Daniela D’Arcangelo , Anna Di Carlo , Sveva Romani , Guido 2 2 2 1 4 Melillo , Antonella Mangoni , Chiara Bertolami , Giulio Pompilio , Antonia Germani , Maurizio C. Capogrossi2* 1 Laboratorio di Biologia Vascolare e Medicina Rigenerativa, Centro Cardiologico Monzino-Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy, 2 Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’Immacolata-IRCCS, Rome, Italy, 3 Mendel Laboratory, Casa Sollievo della Sofferenza-IRCCS, San Giovanni Rotondo, Italy, 4 Fondazione Livio Patrizi, Rome, Italy Abstract Aims: HMGB1 injection into the mouse heart, acutely after myocardial infarction (MI), improves left ventricular (LV) function and prevents remodeling. Here, we examined the effect of HMGB1 in chronically failing hearts. Methods and Results: Adult C57 BL16 female mice underwent coronary artery ligation; three weeks later 200 ng HMGB1 or denatured HMGB1 (control) were injected in the peri-infarcted region of mouse failing hearts. Four weeks after treatment, both echocardiography and hemodynamics demonstrated a significant improvement in LV function in HMGB1-treated mice. Further, HMGB1-treated mice exhibited a ,23% reduction in LV volume, a ,48% increase in infarcted wall thickness and a ,14% reduction in collagen deposition. HMGB1 induced cardiac regeneration and, within the infarcted region, it was found a ,2-fold increase in c-kit+ cell nu