Circulating microparticles from chronic heart failure rats impair migration ability of human umbilical vein endothelial cells

AIM To test the level and protein concentration of circulating microparticles (MPs) in a model of chronic heart failure (HF) rats, and to investigate effect of MPs on migration ability of human umbilical vein endothelial cells (HUVEC). METHODS SD rats were randomly divided into a heart failure group (n=15) and a sham group (n=6). A rat model of abdominal aortic constriction (AAC)-induced cardiac pressure overload was induced. After 12 weeks, changes in cardiac structure and function were evaluated uesing echocardiography and HE staining. Circulating MPs were isolated from rat blood by centrifugation. Total circulating MPs and Annexin Ⅴ(+) MPs were measured by flow cytometry, and the protein concentrations in total MPs were measured by BCA. Cell migration ability was evaluated by the scratch assay. RESULTS The rats after ACC operation showed impaired ventricular function and abnormal myocardial structure comparing to sham rats. Compared with the sham group, left ventricular internal diameter at end-systole (LVIDs) and left ventricular internal diameter at end-diastole (LVIDd) were significantly increased (both P<0.01), and left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly decreased (both P<0.01), proving that chronic heart failure rat model was established successfully. HF rats demonstrated significant higher numbers of both total circulating MPs and Annexin V(+) MPs (both P<0.01), and protein concentration in total circulating MPs increased significantly when compared to the sham group (P<0.01). HUVEC migration ability was significantly impaired after treatment with circulating MPs from heart failure rats at 24 h (P<0.05), and further decreased after 36 h and 48 h treatment (P<0.01). CONCLUSION The level of both circulating MPs and protein concentration in MPs increased in the rats with heart failure. Moreover, the migration ability of HUVEC was significantly impaired by circulating MPs from heart failure rats.