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Myocardial injection with apelin‐overexpressing bone marrow cells improves cardiac repair and systolic function after myocardial infarction
Author(s) -
Chen JianXiong,
Li lanfang,
Zeng heng
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1217.35
Subject(s) - apelin , medicine , cardiac function curve , myocardial infarction , sirt3 , cardiology , bone marrow , angiogenesis , endocrinology , heart failure , receptor , chemistry , sirtuin , biochemistry , acetylation , gene
Our study showed that apelin increases vascular progenitor cell recruitment and promotes cardiac repair after myocardial infarction (MI). However, the effect of apelin on bone marrow cells (BMCs) therapy after MI remains unknown. To investigate whether overexpression of apelin in BMCs improves cell therapy and accelerates cardiac repair and systolic functional recovery in post‐ MI mice. Mouse MI was achieved by coronary artery ligation and BMCs overexpressing apelin (apelin‐BMCs), GFP (GFP‐BMCs) or saline were injected into ischemic area immediately after MI. Apelin receptor (APJ+)/c‐kit+/Sca1+ cells, sirtuin3 (Sirt3) expression and reactive oxygen species (ROS) were assessed. Intramyocardial delivery of apelin‐BMCs led to a significant increase in APJ+/c‐kit+/Sca1+ cells in ischemic area compared to GFP‐BMCs or saline‐treated mice. Apelin‐BMCs treatment led to a significant increase in Sirt3 expression and suppression of ROS formation. Apelin‐BMCs treatment significantly increased angiogenesis and attenuated cardiac scar formation in post‐MI. Most importantly, treatment with apelin‐BMCs significantly improved left ventricular (LV) systolic function, whereas knockout of Sirt3 blunted apelin‐BMCs‐mediated improvement of cardiac repair and systolic functional recovery. Apelin may increase number of APJ+/c‐kit+/Sca1+ cells and improve BMCs therapy after MI via upregulation of Sirt3.