English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Hsa_circ_0054633 has been found to be elevated in the blood of coronary artery disease (CAD) patients. However, the molecular mechanism and the role of hsa_circ_0054633 in the pathogenesis of CAD have not been reported in detail.    Material and methods  The expression of hsa_circ_0054633, microRNA (miR)-107 and thioredoxin-interacting protein (TXNIP) mRNA was measured using quantitative real-time polymerase chain reaction. Human artery vascular smooth muscle cell (HA-VSMC) proliferation, cell cycle, and migration were detected by cell counting kit-8 assay, flow cytometry and transwell assay, respectively. The generation of reactive oxygen species (ROS) was analyzed by dichlorofluorescein diacetate (DCFH-DA) assay. Western blot was utilized to determine the levels of proliferating cell nuclear antigen (PCNA), cyclin D1, matrix metallopeptidase 9 (MMP-9), Mn-superoxide dismutase (SOD2) and TXNIP protein. The interaction between miR-107 and hsa_circ_0054633 or TXNIP was confirmed by dual-luciferase reporter, RNA immunoprecipitation assay or pull-down assay.    Results  Hsa_circ_0054633 was elevated in the plasma of CAD patients, and might be a potential blood biomarker for CAD prediction. Hsa_circ_0054633 silencing reversed PDGF-BB-induced promotion on HA-VSMC proliferation, cell cycle, migration and ROS production. MiR-107 directly interacted with hsa_circ_0054633 and TXNIP, and hsa_circ_0054633 regulated TXNIP expression by sponging miR-107. Besides, rescue assay indicated that the action of hsa_circ_0054633 silencing on PDGF-BB-treated HA-VSMCs could be attenuated by miR-107 inhibition or TXNIP overexpression, respectively.    Conclusions  Hsa_circ_0054633 knockdown protected HA-VSMCs against PDGF-BB-induced dysfunction through regulating miR-107/TXNIP axis, suggesting a potential therapeutic target for coronary atherosclerosis.

Hsa_circ_0054633 regulates PDGF-BB-induced proliferation, migration and oxidative stress of vascular smooth muscle cells through miR-107/TXNIP axis