Abstract 18111: The Adipokine Resistin-Like Molecule Alpha Potentiates Angiogenesis in Heart Failure Mice Model the Adipokine Resistin-Like Molecule Alpha Potentiates Angiogenesis in Heart Failure Mice Model

Introduction: Resistin-like molecule alpha (Retnla) is a marker for anti-inflammatory macrophages. The vital roles of retnla were studied in atherosclerosis, however, the role in heart failure remained unknown. We demonstrated a novel role of retnla regarding angiogenesis in heart failure model. Methods: Heart failure was induced by ligation of left anterior descending artery of wild type (WT) and retnla knockout (KO) mice. Cardiac function was assessed by echocardiography at 8 weeks and cardiac macrophages were analyzed by FACS. Angiogenesis was assessed by tube formation, aortic ring assay, immunohistochemical staining, and microfil-perfusion. Results: Cardiac function was significantly preserved in the retnla KO group 8 weeks after MI. Infiltrated macrophages in the infarcted myocardium were isolated and the number of cardiac macrophages was higher in the KO mice than in the WT mice. On the other hand, there was no statistical difference in macrophage phenotypes. Importantly, we found angiogenesis was substantially increased in the retnla KO group. Microfil-perfused heart images also showed dense distribution of vasculatures in the peri-infarct zone of KO mouse. To compare the intrinsic angiogenesis capacity, we isolated bone-marrow derived mesenchymal stem cells, and tube formation was better in the retnla KO groupp. Aortic rings from retnla KO mice had a significantly increased sprouting capacity compared with WT mice. Conclusions: These findings illustrate that enhanced angiogenesis-related events in retnla KO mice are associated with cardioprotection in heart failure. Bone marrow-stem cells recruited to the heart may contribute to increased angiogenesis, and intensive studies to suggest the potent therapeutic mediators to reverse cardiac failure are under way in terms of the novel function of retnla in the cardiac pathology.