ArticleMedical science monitor : international medical journal of experimental and clinical research2020
MicroRNA-328-3p Protects Vascular Endothelial Cells Against Oxidized Low-Density Lipoprotein Induced Injury via Targeting Forkhead Box Protein O4 (FOXO4) in Atherosclerosis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- New Biomarkers in the Diagnosis and Prognosis of Dilated Cardiomyopathy: Pro-Resolving Lipids and miRNAs.Cells · 2025Article
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- CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022Review
- The comprehensive detection of miRNA and circRNA in the regulation of intramuscular and subcutaneous adipose tissue of Laiwu pig.Scientific reports · 2022Article
- Circulating microRNAs as putative mediators in the association between short-term exposure to ambient air pollution and cardiovascular biomarkers.Ecotoxicology and environmental safety · 2022Article
- Circulating microRNAs in patients with aneurysmal dilatation of coronary arteries.Experimental and therapeutic medicine · 2022Article
- Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Zhilong Huoxue Tongyu Capsule Alleviated the Pyroptosis of Vascular Endothelial Cells Induced by ox-LDL through miR-30b-5p/NLRP3.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to enhance WNT4 expression.Bioengineered · 2021Article
- miR-328a-3p stimulates endothelial cell migration and tubulogenesis.Experimental and therapeutic medicine · 2021Article
- Circ_0004104 knockdown alleviates oxidized low-density lipoprotein-induced dysfunction in vascular endothelial cells through targeting miR-328-3p/TRIM14 axis in atherosclerosis.BMC cardiovascular disorders · 2021Article
- Simvastatin inhibits POVPC-mediated induction of endothelial-to-mesenchymal cell transition.Journal of lipid research · 2021Article
- miR-328-3p, a Predictor of Stroke, Aggravates the Cerebral Ischemia-Reperfusion Injury.International journal of general medicine · 2021Article
- circ_0003204 Regulates Cell Growth, Oxidative Stress, and Inflammation in ox-LDL-Induced Vascular Endothelial Cells via Regulating miR-942-5p/HDAC9 Axis.Frontiers in cardiovascular medicine · 2021Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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