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Few studies have addressed the mechanism by which circ_0010729 regulates hypoxia-induced cell injury in cardiovascular diseases. However, its role and its regulatory mechanism in myocardial infarction remain to be explored. Cell viability, cycle, apoptosis, and migration were analyzed using cell counting kit-8 assay, flow cytometry, caspase-3 activity assay kit and transwell assay, respectively. Tumor necrosis factor-α (TNF-α), and inter-leukin-6 (IL-6) concentrations were examined by enzyme-linked immunosorbent assay. Glucose metabolism was calculated by detecting ATP production, glucose uptake and lactate production. Levels of circ_0010729, miR-370-3p and TNF Receptor Associated Factor 6 (TRAF6) were detected using quantitative real-time polymerase chain reaction or western blot. The direct interaction between circ_0010729 and TRAF6 or miR-370-3p was verified using dual-luciferase reporter assay and RNA immunoprecipitation assay. Under hypoxia condition, cardiomyocytes suffered from cell viability suppression, cell cycle arrest, cell apoptosis promotion, migration reduction, increase of inflammatory factor IL-6 and TNF-α, as well as glycolysis inhibition. Circ_0010729 expression was up-regulated in the cardiomyocytes at different hypoxia-exposed time points. Circ_0010729 knockdown protected cardiomyocytes against hypoxic dysfunction, while circ_0010729 overexpression showed inverse effects. MiR-370-3p was confirmed to directly bind to circ_0010729 or TRAF6. MiR-370-3p inhibition attenuated the protective effects of circ_0010729 knockdown on hypoxia-modulated cardiomyocyte dysfunction. MiR-370-3p restoration protected cardiomyocytes against hypoxic injury via targeting TRAF6. Besides, circ_0010729 in-directly regulated TRAF6 expression via miR-370-3p. This study demonstrated that circ_0010729 knockdown attenuated hypoxia-induced cardiomyocyte dysfunction via miR-370-3p/TRAF6 axis, indicating a potential therapeutic target for myocardial infarction. [ABSTRACT FROM AUTHOR]

With the improvement of people's living standards and change of lifestyles, the morbidity of the cardiovascular and cerebrovascular diseases (cardiovascular and cerebrovascular diseases, CCVD), especially the atherosclerosis (atherosclerosis, AS), presents a rising tendency year by year. The injury and inflammatory reaction of endothelial cells is one of the important factors causing AS. However, its molecular mechanism still needs further studying. This paper will discuss the influence of hemodynamics on the cardiac muscle cells cardiac index and its molecular mechanism, the Human umbilical vein endothelial cells (Human umbilical vein endothelial cells, HUVEC) were cultivated and separated and processed by lOOng Lipopolysaccharide (Lipopolysaccharide, LPS) to simulate the injury and inflammation state of the vascular endothelial cells. The hemodynamic state was simulated by the Parallel- Plate Flow Chamber in laboratory. And the MTT was adopted to detect HUVEC growth and the flow cytometry (flow cytometry, FCT) to detect HUVEC apoptosis. And the cardiac index was tested by RT-PCR and western blot. And the cell apoptosis caused by LPS was tested when the cardiac index was over-expressed and reduced. LPS could inhabit HUVEC growth and lead to its apoptosis. Hemodynamics (16dyn/cm2) could reduce HUVEC growth inhibition and apoptosis caused by LPS. And the dose-dependent LPS reduced HUVEC cardiac index, while when it was processed by the hemodynamics (16dyn/cnr), the HUVEC cardiac index would increase. And the over-expression of the cardiac index could inhabit the cell apoptosis caused by LPS, and the interference technology was adopted to deal with the cardiac index, which could enhance the cell apoptosis caused by LPS. Hemodynamics could inhabit the HUVEC apoptosis caused by LPS, which might be one of the reasons causing AS, through enhancing the cardiac index. [ABSTRACT FROM AUTHOR]