ArticleJournal of cellular and molecular medicine2020
LncRNA TUG1 regulates ApoM to promote atherosclerosis progression through miR-92a/FXR1 axis.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- Advances in the Regulation of Lipid Metabolism by Non-Coding RNAs.Animals : an open access journal from MDPI · 2025Review
- Gene Therapy Approaches for Atherosclerosis Focusing on Targeting Lipid Metabolism and Inflammation.International journal of molecular sciences · 2025Review
- LncRNA MEG3 independently collaborates with lncRNA TUG1 to prevent cholesterol efflux in ox-LDL-induced human umbilical vein endothelial cells.Molecular biology reports · 2025Article
- The Role of Selected lncRNAs in Lipid Metabolism and Cardiovascular Disease Risk.International journal of molecular sciences · 2024Review
- Advances in applications of artificial intelligence algorithms for cancer-related miRNA research.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Review
- The Mechanisms of miRNAs on Target Regulation and their Recent Advances in Atherosclerosis.Current medicinal chemistry · 2024Review
- Role of Macrophage lncRNAs in Mediating Inflammatory Processes in Atherosclerosis and Sepsis.Biomedicines · 2023Review
- Current advancements and future perspectives of long noncoding RNAs in lipid metabolism and signaling.Journal of advanced research · 2023Review
- Review
- The Role of the VEGF Family in Atherosclerosis Development and Its Potential as Treatment Targets.International journal of molecular sciences · 2022Review
- Foam Cells in Atherosclerosis: Novel Insights Into Its Origins, Consequences, and Molecular Mechanisms.Frontiers in cardiovascular medicine · 2022Review
- Genomic Variants and Multilevel Regulation ofJournal of cardiovascular development and disease · 2021Review
- Long Noncoding RNAs: Novel Important Players in Adipocyte Lipid Metabolism and Derivative Diseases.Frontiers in physiology · 2021Review
- LncRNATUG1 Facilitates Th2 Cell Differentiation by Targeting the miR-29c/B7-H3 Axis on Macrophages.Frontiers in immunology · 2021Article
- lncRNAInternational journal of clinical and experimental pathology · 2021Article
- Long Non-Coding RNA Associated with Cholesterol Homeostasis and Its Involvement in Metabolic Diseases.International journal of molecular sciences · 2020Review
- LncRNA TUG1 regulates ApoM to promote atherosclerosis progression through miR-92a/FXR1 axis.Journal of cellular and molecular medicine · 2020Article
- Functioning of Long Noncoding RNAs Expressed in Macrophage in the Development of Atherosclerosis.Frontiers in pharmacology · 2020Review
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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
This study aims to explore the possible mechanism of TUG1 regulating ApoM in AS. To this end, expression levels of TUG1 and ApoM were measured in high fat dieted C57BL/6J mice, normal dieted C57BL/6J mice, ob/ob mice and db/db mice. LV-TUG1 or sh-TUG1 was injected into C57BL/6J mice before isolating peritoneal macrophages to measure cholesterol efflux (CE) and expression levels of ABCA1, ABCG1 and SR-BI. Meanwhile, CE in RAW264.7 cells was also measured after cell transfection. Dual luciferase reporter assay and anti-AGO2 RIP were applied to verify the relationship among TUG1, FXR1 and miR-92a. Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterin (LDL-C), high-density lipoprotein cholesterol (HDL-C) as well as expressions of inflammatory cytokines (TNF-α, IL-1β and IL-6) in plasma were measured. Knock-down or expressed TUG1, FXR1 or miR-92a in NCTC 1469 cells or in ApoE-/- AS mice to determine the alteration on ApoM and plaque size. TUG1 was highly expressed while ApoM was down-regulated in high fat dieted C57BL/6J mice, b/ob and db/db mice. Overexpression of TUG1 could reduce the expression of ApoM, ABCA1 and ABCG1 in addition to slowing down CE rate. Reversed expression pattern was found in cells with knock-down of TUG1. TUG1 can compete with FXR1 to bind miR-92a. FXR1 negatively target ApoM. Overexpression of TUG1 in ApoE-/- mice can increase plaque size and enhance macrophage contents accordingly. TUG1 can inhibit ApoM in both liver tissues and plasma to inhibit CE through regulating miR-92a/ FXR1 axis. TUG1 is a promising target for AS treatment.
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