These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: CircRSF1 contributes to endothelial cell growth, migration and tube formation under ox-LDL stress through regulating miR-758/CCND2 axis.
    Author: Wei Z, Ran H, Yang C.
    Journal: Life Sci; 2020 Oct 15; 259():118241. PubMed ID: 32791147.
    Abstract:
    AIMS: Compelling evidences demonstrate that informative RNAs play essential role in therapy of atherosclerosis. Here, we attempted to study the role of hsa_circ_0000345 (circRSF1) in endothelial cell damage through competing endogenous RNA pathway. MATERIALS AND METHODS: Expression of circRSF1, miRNA-758-3p (miR-758) and cyclin D2 (CCND2) was detected using RT-qPCR and western blotting, and the cross-talk among them was identified using dual-luciferase reporter assay and RNA immunoprecipitation. The low-density lipoprotein cholesterol (LDL-C) level was measured with enzyme-linked immunosorbent assay. Cell growth was measured by MTS assay, flow cytometry and caspase-3 activity assay kit. Migration and tube formation were determined by scratch migration assay and tube formation assay, respectively. KEY FINDINGS: CircRSF1 and CCND2 were downregulated, whereas miR-758 was upregulated in serum of patients with atherosclerosis and oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs). Moreover, levels of circRSF1, miR-758 and CCND2 were correlated with circulating LDL-C level. Restoring circRSF1 and silencing miR-758 could improve cell viability, tube formation and migration of HAECs under ox-LDL treatment, as well as attenuated apoptotic rate and caspase-3 activity. However, miR-758 upregulation counteracted the promotion of circRSF1 on cell growth, migration and tube formation in ox-LDL-induced HAECs; so did CCND2 deletion on effect of miR-758 silence. Notably, circRSF1 and CCND2 could competitively bound to miR-758, and circRSF1 positively regulated CCND2 expression via miR-758. SIGNIFICANCE: CircRSF1 could protect against ox-LDL-induced endothelial cell injury in vitro via miR-758/CCND2 axis, suggesting circRSF1 as a potential target for the treatment of atherosclerosis.
    [Abstract] [Full Text] [Related] [New Search]