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Proliferation of vascular smooth muscle cells (VSMCs) plays an important role in various vascular diseases. Abnormal hemodynamic factors are important stimulus for promoting proliferation of VSMCs. In this study, we show that transmural pressure (TP) promotes the proliferation of human arterial smooth muscle cells (HASMCs) and its related mechanism. HASMCs were treated with different TPs (0,100,120,140,160,180 and 200 mmHg) in a custom-made pressure loading apparatus for 6 h. Results showed that proliferation of HASMCs was significantly promoted when the TP was over 160 mmHg compared with 0 mmHg (atmosphere pressure). In like manner, the expressions of NADPH oxidase 2(Nox2) and Survivin (SVV) and production of intracellular reactive oxygen species (ROS) were all elevated distinctly when TP exceeded 160 mmHg. Moreover, ROS scavenger NAC reduced TP-induced proliferation of HASMCs and expression of SVV largely, and slightly down-regulated expression of NOX2. NOX inhibitor apocynin (Apo) also significantly reduced TP-induced proliferation of HASMCs and expression of SVV and almost completely eliminated TP-induced production of ROS. These results demonstrate that TP drives proliferation of HASMCs via mechanism associated with NOX and SVV., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objective To assess the effects of survivin (SVV)in vascular endothelial cells. Methods In this study, we applied a gain-of-function approach and ectopically expressed SVV in rat aortic endothelial cells (RAECs) using a SVV-expressing adenovirus. The resulting SVV expression on the steady-state mRNA and protein level in RAECs was determined by reverse transcription quantitative PCR and Western blot, respectively. Cell viability, apoptosis, and migration were assessed in vitro by CCK-8 assay, flow cytometry, and transwell assay, respectively. The effect of SVV on in vivo angiogenesis was evaluated by immunohistochemistry in nude mice. Non-infected RAECs and those infected with GFP-expressing control adenovirus were used as controls. Results Compared to non-infected or control adenovirus-infected RAECs in vitro , SVV-expressing cells had increased viability and migratory capability, but reduced apoptosis . In vivo , SVV-expressing RAECs were associated with a higher level of angiogenesis. Conclusion SVV is a positive regulator of endothelial cell survival and migration, and thus, stabilizes endothelial cells and stimulates angiogenesis. [ABSTRACT FROM AUTHOR]