ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Oxidized Low Density Lipoprotein-Induced Atherogenic Response of Human Umbilical Vascular Endothelial Cells (HUVECs) was Protected by Atorvastatin by Regulating miR-26a-5p/Phosphatase and Tensin Homolog (PTEN).
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.Molecular and cellular biochemistry · 2025Review
- Dental Pulp Stem Cells Attenuate Early Brain Injury After Subarachnoid Hemorrhage via miR-26a-5p/PTEN/AKT Pathway.Neurochemical research · 2025Article
- Polydatin reverses oxidation low lipoprotein (oxLDL)-induced apoptosis of human umbilical vein endothelial cells <em>via</em> regulating the miR-26a-5p/BID axis.European journal of histochemistry : EJH · 2022Article
- Correlation Between Serum β2-GPI/oxLDL and the Risk of Cerebral Infarction in Patients with T2DM.Frontiers in surgery · 2022Article
- Atorvastatin Restores PPARα Inhibition of Lipid Metabolism Disorders by Downregulating miR-21 Expression to Improve Mitochondrial Function and Alleviate Diabetic Nephropathy Progression.Frontiers in pharmacology · 2022Article
- LncRNA GAS5 as miR-26a-5p Sponge Regulates the PTEN/PI3K/Akt Axis and Affects Extracellular Matrix Synthesis in Degenerative Nucleus Pulposus CellsFrontiers in neurology · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Atherosclerosis is a chronic and multifactorial disease, and it is the main reason of coronary heart disease, cerebral infarction, and peripheral vascular disease, which leads to the formation of lesions in arterial blood vessels. Our study aimed to explore the protective effect and its underlying mechanism of atorvastatin (ATV) on oxidized low-density lipoprotein (ox-LDL)-induced atherosclerosis. MATERIAL AND METHODS Human umbilical vascular endothelial cells (HUVECs) were cultured and pretreated with ox-LDL to establish an in vitro atherosclerotic cell model. Cell Counting Kit-8 (CCK-8) assay, TUNEL staining, and Transwell assay were used to detect the cell activity, apoptosis, and migration in HUVECs. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were applied to measure the mRNA and protein expressions of adhesion-related genes in HUVECs. RESULTS Pretreated with 100 mg/L ox-LDL resulted in a 57.23% decrease of cell viability and 81.09% increase of apoptotic injury in HUVECs compare to the control. Meanwhile, ox-LDL pretreatment increased the cell migration and the expression of miR-26a-5p in HUVECs. ATV treatment could effectively reverse the cellular damage induced by ox-LDL, decrease the release of adhesion-related molecules, and downregulate the expression of miR-26a-5p by 44.79% in HUVECs. Moreover, phosphatase and tensin homolog (PTEN) was demonstrated to be the target gene of miR-26a-5p. CONCLUSIONS Our results highlight that ATV protects against ox-LDL-induced downregulation of cell viability, upregulation of cell apoptosis, migration, as well as the release of adhesion-related molecules in HUVECs through the miR-26a-5p/PTEN axis. This study provides new insights into the underlying mechanism of ATV therapeutic potential in atherosclerosis, and also provides a new strategy for the treatment of atherosclerosis.
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