ArticleKorean circulation journal2025
LncRNA uc003pxg.1 Interacts With miR-339-5p Promote Vascular Endothelial Cell Proliferation, Migration and Angiogenesis.
Article in Korean circulation journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Exosomal lncRNAs in Cerebrovascular Diseases: Biomarkers, Pathological Mechanisms, and Therapeutic Potential.Non-coding RNA · 2026Review
- Review
- Epigenetic Regulation of Endothelial-Mesenchymal Transition in Vascular Atherosclerosis Development.Korean circulation journal · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
BACKGROUND AND
objectivesThis study aimed to investigate the roles of lncRNA uc003pxg.1 and miR-339-5p in regulating the occurrence and development of coronary heart disease.
methodsFirst, the expression levels of uc003pxg.1 and miR-339-5p were verified in peripheral blood mononuclear cells of clinical samples. Then, the target gene was identified using high-throughput sequencing combined with bioinformatics. Human umbilical vein endothelial cells (HUVECs) were transfected with si-uc003pxg.1, miR-339-5p mimic and miR-339-5p inhibitor, and the expression of related genes was detected by reverse transcription-quantitative polymerase chain reaction and western blotting. EdU, CCK-8, Cell scratch and Transwell assays were used to analyze the effects of uc003pxg.1 and miR-339-5p on cell proliferation and migration.
resultsThe expression of uc003pxg.1 and miR-339-5p was negatively correlated in clinical samples and HUVECs. The si-uc003pxg.1 and miR-339-5p mimic decreased the proliferation and migration of HUVECs and decreased the expression of transforming growth factor (TGF)-β1 and α-smooth muscle actin (SMA). The protein expression levels of TGF-β1, α-SMA, CD31, collagen I, collagen III and endoglin were decreased, and angiogenesis was weakened. The miR-339-5p inhibitor had the opposite effect.
conclusionsOur study revealed that upregulation of uc003pxg.1 and downregulation of miR-339-5p in vitro promote cell proliferation, cell migration and angiogenesis and upregulate the expression of TGF-β1, α-SMA, CD31, collagen I, collagen III and endoglin, which may lead to the development of vascular atherosclerosis.
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