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

BACKGROUND Endothelial cell (EC) injury is underlies for the pathogenesis of atherosclerosis (AS). MicroRNAs (miRNAs) have been indicated play important role in modulating AS occurrence and development. However, how miR-328-3p modulates EC injury molecular level for AS remains unclear. MATERIAL AND METHODS MiR-328-3p and forkhead box protein O4 (FOXO4) expression were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell viability was analyzed by Cell Counting Kit-8 (CCK-8) assay. Flow cytometry was utilized to analyze the apoptotic rate. The migration and invasion abilities were measured by Transwell assay. Western blot was applied to examine the expression of C-caspase 3, Beclin, LC3-I, and LC3-II. The levels of interleukin (IL)-1ß, IL-10, and tumor necrosis factor-alpha (TNF-alpha) were tested by enzyme-linked immunosorbent assay (ELISA) assay and western blot. RESULTS MiR-328-3p expression was downregulated in oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs). Overexpressed miR-328-3p obviously alleviated ox-LDL induced inhibition on cell viability, migration and invasion, stimulation on apoptosis, autophagy as well as inflammation in HUVECs. FOXO4 was elevated in ox-LDL HUVECs, and functional assay indicated that FOXO4 aggravated ox-LDL induced HUVECs impairment. In addition, FOXO4 was a target of miR-328-3p in HUVECs; rescue experiments suggested miR-328-3p could protect HUVECs against ox-LDL induced injury via regulating FOXO4. CONCLUSIONS MiR-328-3p protected vascular endothelial cells against ox-LDL induced injury via targeting FOXO4, suggesting a novel insight for atherosclerosis treatment.

medical science monitor

MicroRNA-328-3p Protects Vascular Endothelial Cells Against Oxidized Low-Density Lipoprotein Induced Injury via Targeting Forkhead Box Protein O4 (FOXO4) in Atherosclerosis