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The proliferation and migration of vascular smooth muscle cells (VSMCs) are one of the key regulatory links of atherosclerosis (AS). Long noncoding RNAs (lncRNAs) are emerging as key regulators in AS development. In this study, we first assessed the expression level of smooth muscle and endothelial cell-enriched migration/differentiation-associated lncRNA (SENCR) in the plasma of patients with coronary heart disease (CHD) and its predictive and diagnostic value. Second, we investigated the role of SENCR in the regulation network of human aortic-VSMCs (HA-VSMCs) proliferation and migration and determined its downstream regulatory mechanism. The results showed that SENCR was downregulated in the peripheral blood of CHD, and negatively related to the Gensini score. SENCR was enriched in HA-VSMCs and mainly distributed in cytoplasm. Overexpression of SENCR significantly inhibited HA-VSMCs proliferation, migration, and block cell cycle, while the knockdown of SENCR had the opposite effects. Moreover, bioinformatics analysis and luciferase reporter assay demonstrated that miR-4731-5p could directly bind to SENCR. Besides, we proved that FOXO3a inhibited HA-VSMCs proliferation and migration by binding to the 3'-untranslated region of miR-4731-5p. In summary, our research suggested that SENCR affects HA-VSMCs proliferation and migration via regulating the miR-4731-5p/FOXO3a pathway.

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 100ng 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/cm