ArticleThrombosis journal2022
Long noncoding RNA TUG1 induces angiogenesis of endothelial progenitor cells and dissolution of deep vein thrombosis.
Article in Thrombosis journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- The Role of Circulating MicroRNAs as Biomarkers and Therapeutic Targets in Venous Thromboembolism: A Systematic Review.Journal of clinical medicine · 2026Review
- Pathological, diagnostic, and therapeutic implications of non-coding RNAs in deep vein thrombosis: A comprehensive review.Journal of thrombosis and thrombolysis · 2026Review
- Article
- Clinical significance and underlying mechanism of long non-coding RNA SNHG12 in lower extremity deep venous thrombosis.Clinical and translational science · 2024Article
- Serum lncRNA RAMP2-AS1 Served as a Biomarker of Deep Vein Thrombosis Occurrence and Development in Elderly.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024Article
- Long Non-Coding RNAs: Bridging Cancer-Associated Thrombosis and Clinical Outcome of Ovarian Cancer Patients.International journal of molecular sciences · 2023Article
- Long Non-Coding RNAs in Venous Thromboembolism: Where Do We Stand?International journal of molecular sciences · 2023Review
- LINC00659 exacerbates endothelial progenitor cell dysfunction in deep vein thrombosis of the lower extremities by activating DNMT3A-mediated FGF1 promoter methylation.Thrombosis journal · 2023Article
- LncRNA NEAT1 Promotes Vascular Endothelial Cell Dysfunction via miR-218-5p/GAB2 and Serves as a Diagnostic Biomarker for Deep Vein Thrombosis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLong non-coding RNA (lncRNA) essentially controls many physiological and pathological processes of deep vein thrombosis (DVT). Based on that, lncRNA taurine upregulated gene 1 (TUG1)-involved angiogenesis of endothelial progenitor cells (EPCs) and dissolution of DVT was explored.
methodsIn the in-vitro experiments, EPCs were engineered with mimic, inhibitor, siRNA, and plasmid, after which tube formation, proliferation, migration, and apoptosis were checked. In the in-vivo experiments, a DVT mouse model was established. Before the DVT operation, the mice were injected with agomir, antagomir, siRNA, and plasmid. Subsequently, thrombosis and damage to the femoral vein were pathologically evaluated. TUG1, miR-92a-3p, and 3-Hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr) expression in the femoral vein was tested. The relationship between TUG1, miR-92a-3p, and Hmgcr was validated.
resultsDVT mice showed suppressed TUG1 and Hmgcr expression, and elevated miR-92a-3p expression. In EPCs, TUG1 overexpression or miR-92a-3p inhibition promoted cellular angiogenesis, whereas Hmgcr silencing blocked cellular angiogenesis. In DVT mice, elevated TUG1 or inhibited miR-92a-3p suppressed thrombosis and damage to the femoral vein whilst Hmgcr knockdown acted oppositely. In both cellular and animal models, TUG1 overexpression-induced effects could be mitigated by miR-92a-3p up-regulation. Mechanically, TUG1 interacted with miR-92a-3p to regulate Hmgcr expression.
conclusionEvidently, TUG1 promotes the angiogenesis of EPCs and dissolution of DVT via the interplay with miR-92a-3p and Hmgcr.
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