Abstract 9905: Myeloid Cell Derived Leucine Rich α2 Glycoprotein Attenuates Adverse Cardiac Remodeling After Myocardial Infarction

• Published in: Circulation (New York, N.Y.) N.Y.), 2015-11, Vol.132 (Suppl_3 Suppl 3), p.A9905-A9905
• Main Authors: Kumagai, Shohei, Nakayama, Hiroyuki, Fujimoto, Minoru, Honda, Hiromi, Serada, Satoshi, Kasai, Atsushi, Obana, Masanori, Sakata, Yasushi, Sawa, Yoshiki, Naka, Tetsuji, Fujio, Yasushi
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.132.suppl_3.9905

BackgroundLeucine rich α2 glycoprotein (LRG), a member of the leucine-rich repeat family, was isolated from human plasma. Recently, LRG has been identified as a novel serum biomarker for various inflammatory diseases. It was also reported that serum LRG concentrations was strongly correlated with B-type natriuretic peptide in patients with heart failure. However, its pathophysiological roles in hearts after myocardial infarction (MI) remain to be elucidated.ObjectiveTo determine the functional roles of LRG in cardiac remodeling after MI.Methods and ResultsMurine MI was generated by ligating the left coronary artery. The expression of LRG was increased in hearts after MI. Immunofluorescence microscopic and flow cytometric analyses revealed that LRG was mainly produced by CD11b-positive myeloid cells in post-infarct myocardium. To elucidate pathophysiological roles of LRG in heart, we generated MI in wild-type (WT) and LRG-knockout (KO) mice. At day 14 after MI, cardiac fibrosis and dysfunction were aggravated in KO mice compared to WT mice (fibrotic area/ LV areaWT34.1 ± 7.2%, KO46.5 ± 12.8% n=10-16, p