ArticleMolecular medicine (Cambridge, Mass.)2020
THRIL mediates endothelial progenitor cells autophagy via AKT pathway and FUS.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- LncRNA-Protein Interactions: A Key to Deciphering LncRNA Mechanisms.Biomolecules · 2025Review
- LncRNA MIR4697HG Alleviates Endothelial Cell Injury and Atherosclerosis Progression in Mice via the FUS/ANXA5 Axis.Biochemical genetics · 2024Article
- Sequential changes in expression of long non-coding RNAs THRIL and MALAT1 after ischemic stroke.Current journal of neurology · 2024Article
- Role of LncRNAs in the Pathogenesis of Coronary Artery Disease.Reviews in cardiovascular medicine · 2023Review
- LncRNA THRIL Functions as a Marker for Carotid Artery Stenosis and Affects the Biological Function of Human Aortic Endothelial Cell.Journal of inflammation research · 2023Article
- Article
- LncRNA THRIL promotes high glucose-induced proliferation and migration of human retina microvascular endothelial cells through enhancing autophagy.Acta diabetologica · 2022Article
- Regulation of Endothelial Progenitor Cell Functions in Ischemic Heart Disease: New Therapeutic Targets for Cardiac Remodeling and Repair.Frontiers in cardiovascular medicine · 2022Review
- LncRNAAnnals of translational medicine · 2021Article
- The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction.Frontiers in cardiovascular medicine · 2021Review
- Dysregulated Circulating Apoptosis- and Autophagy-Related lncRNAs as Diagnostic Markers in Coronary Artery Disease.BioMed research international · 2021Article
- Autophagy-Sirtuin1(SIRT1) Alleviated the Coronary Atherosclerosis (AS)in Mice through Regulating the Proliferation and Migration of Endothelial Progenitor Cells (EPCs) via wnt/β-catenin/GSK3β Signaling Pathway.The journal of nutrition, health & agingArticle
- Role of thrombus-derived exosomal lncRNA LOC101928697 in regulating endothelial function via FUS protein interaction in myocardial infarction.Science progressArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study focused on the roles of lncRNA THRIL in coronary atherosclerotic heart disease (CAD) through regulating AKT signaling pathway and directly interacting with FUS.
methodsQRT-PCR was conducted to detect the expression of THRIL in CAD blood samples and endothelial progenitor cells (EPCs). Cell autophagy of EPCs was examined through Cyto-ID Autophagy Detection Kit. CCK-8 assay and flow cytometry were carried out to assess cell viability and apoptosis under various interference conditions. Western blotting was conducted to detect the expression of interest proteins. The expression levels of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were measured by qRT-PCR. The direct interactions between HCG18 and FUS was confirmed through RNA electrophoretic mobility shift assay (RNA EMSA) and RNA immunoprecipitation (RIP) assay.
resultsTHRIL was upregulated in CAD blood samples and EPCs. Knockdown of THRIL in EPCs promoted cell viability, inhibited cell autophagy and further suppressed the development of CAD. Over-expression of THRIL induced inactivation of AKT pathway, while knockdown of THRIL played reversed effects. THRIL directly interacted with FUS protein and knockdown of FUS reversed the over-expressing effect of THRIL on cell proliferation, autophagy and the status of AKT pathway.
conclusionTHRIL inhibits the proliferation and mediates autophagy of endothelial progenitor cells via AKT pathway and FUS.
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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 Socratic graph.