ArticleMolecular and cellular biochemistry2020
LNCRNA OIP5-AS1 regulates oxidative low-density lipoprotein-mediated endothelial cell injury via miR-320a/LOX1 axis.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Silencing of OIP5-AS1 Protects Endothelial Cells From ox-LDL-Triggered Injury by Regulating KLF5 Expression via Sponging miR-135a-5p.Frontiers in cardiovascular medicine · 2021Pooled it
- Impact of biomarkers on carotid artery disease and stroke.Scientific reports · 2025Observational
- Regulatory roles of noncoding RNAs in intervertebral disc degeneration as potential therapeutic targets (Review).Experimental and therapeutic medicine · 2023Review
- Suppression of lncRNA OIP5-AS1 Attenuates Apoptosis and Inflammation, and Promotes Proliferation by Mediating miR-25-3p Expression in Lipopolysaccharide-Induced Myocardial Injury.Analytical cellular pathology (Amsterdam) · 2023Article
- The role of lncRNA OIP5-AS1 in cancer development and progression.Apoptosis : an international journal on programmed cell death · 2022Review
- The mechanisms of glycolipid metabolism disorder on vascular injury in type 2 diabetes.Frontiers in physiology · 2022Review
- Long non-coding RNA OIP5-AS1 (Cyrano): A context-specific regulator of normal and disease processes.Clinical and translational medicine · 2022Review
- LncRNA OIP5-AS1 accelerates intervertebral disc degeneration by targeting miR-25-3p.Bioengineered · 2021Article
- Exosomes released from mesenchymal stem cells overexpressing microRNA-30e ameliorate heart failure in rats with myocardial infarction.American journal of translational research · 2021Article
- Downregulation of microRNA-320a inhibits proliferation and induces apoptosis of retinoblastoma cells via targeting TUSC3.Experimental and therapeutic medicine · 2020Article
- Macrophage Long Non-Coding RNAs in Pathogenesis of Cardiovascular Disease.Non-coding RNA · 2020Review
- LncRNAs Stand as Potent Biomarkers and Therapeutic Targets for Stroke.Frontiers in aging neuroscience · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increasing amount of research showed that endothelial cells (ECs) play crucial role in vascular disorders such as atherosclerosis (AS). LncRNA OIP5-AS1 and microRNA-320a (miR-320a) were reported to exert function in ECs. The purpose of this research was to investigate the functional mechanism of OIP5-AS1 and miR-320a in ox-LDL-treated HUVECs. The RNA levels of OIP5-AS1, miR-320a, and Lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of LOX1 and cell apoptosis-related genes were determined by Western blot assay. In addition, Cell Counting Kit-8 (CCK-8) and flow cytometry analysis were used to assess cell viability and apoptosis, respectively. Lactate dehydrogenase (LDH) activity was measured using LDH release assay. Besides, the interaction between miR-320a and OIP5-AS1 or LOX1 was predicted by starbase and verified by the dual-luciferase reporter assay. OIP5-AS1 expression was increased and miR-320a expression was decreased in oxidative low-density lipoprotein (ox-LDL)-treated HUVECs. OIP5-AS1 knockdown upregulated ox-LDL-treated HUVECs viability and suppressed apoptosis as well as LDH release. Interestingly, OIP5-AS1 elevated LOX1 level through downregulating miR-320a expression. As expected, miR-320a modulated LOX1 expression to mediate ox-LDL-treated HUVECs progression. Furthermore, OIP5-AS1 knockdown modulated cell progression via regulating miR-320a/LOX1 axis in ox-LDL-treated HUVECs. Our results demonstrated that the depletion of OIP5-AS1 enhanced cell viability and repressed apoptosis as well as LDH release in ox-LDL-treated HUVECs, providing potential target for the treatment of AS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.