Abstract 68: Endostatin Promotes Proliferation and Migration of Rat Myofibroblasts Isolated From the Infarcted Area After Myocardial Infarction
Background: Endostatin, a 20 kDa non-collagenous fragment of type XVIII collagen, is known as an endogenous anti-angiogenic factor. In the heart tissues of experimental heart failure models, such as cardiac hypertrophy and myocardial infarction, the expression levels of endostatin increase. Proliferation, migration and collagen synthesis of myofibroblasts are important processes during the tissue remodeling in injury sites after myocardial infarction. However, the effects of endostatin on cardiac myofibroblasts have not been clarified. We investigated the effect of endostatin on the functions of myofibroblasts isolated from infarcted myocardial tissues of rat.
Methods and Results: Left ventricular myocardial infarction was induced by ligation the left anterior descending coronary artery of male Wistar rats. The infarcted myocardial tissues were harvested 2 weeks after the operation and placed on the culture plate with serum-containing medium. Migrated cells from the tissues were isolated and used as myofibroblasts. High expression of α-smooth muscle actin, vimentin and type I collagen in these cells were confirmed by immunofluorescence staining. Cell counting assay was performed to determine a cell proliferation. Endostatin (100-3000 ng/ml, 48 h) increased the proliferation of myofibroblasts. Boyden chamber assay was performed to measure a cell migration. Endostatin (300-3000 ng/ml, 24 h) stimulated the migration of myofibroblasts. Western blotting was performed to measure a secretion of type I collagen. Endostatin (100-3000 ng/ml, 24 h) had no influence on it.
Conclusions: These data suggest that endostatin might promote scar formation after myocardial infarction through the activation of proliferation and migration of myofibroblasts.
Author Disclosures: M. Okada: None. Y. Hirano: None. H. Yamawaki: None.
- © 2015 by American Heart Association, Inc.