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Background <p>The current research aims to clarify the clinical significance and molecular function of long-non-coding RNA growth arrest-specific 5 (GAS5) in deep vein thrombosis (DVT).</p> Methods <p>92 DVT patients and 86 controls were included in this study. Real-time quantitative reverse transcription PCR (RT-qPCR) was performed to measure GAS5, microRNA (miR)-134-5p, and forkhead box protein 3 (FOXP3) levels. Receiver operating characteristic (ROC) curves evaluated the diagnostic significance of GAS5 in DVT. Kaplan-Meier and Cox regression analyses assessed the prognostic significance of post-thrombotic syndrome (PTS). An in vitro model using CoCl<sub>2</sub>-induced HUVECs was established to measure cell proliferation, apoptosis, adhesion factors, and inflammatory factors via Cell Counting Kit-8 (CCK-8), flow cytometry, RT-qPCR, and Enzyme-linked immunosorbent assay (ELISA). Protein expression of FOXP3, HIF-1α, and VEGFA was evaluated via Western blot. Dual luciferase report, RIP, and RNA pull-down assays confirmed the direct binding of miR-134-5p to GAS5 or FOXP3.</p> Results <p>GAS5 and FOXP3 were downregulated in DVT patients’ serum and CoCl<sub>2</sub>-induced HUVECs, while miR-134-5p was upregulated. GAS5 distinguished DVT patients from controls with 89.13% sensitivity and 83.72% specificity. At 18-month follow-up, 32.60% of patients developed PTS, which was more common among those with low GAS5 expression. Mechanistically, GAS5 and FOXP3 bind to miR-134-5p. CoCl<sub>2</sub> enhanced the protein levels of HIF-1α and VEGFA. Higher GAS5 levels reduced CoCl<sub>2</sub>-induced proliferation suppression, apoptosis promotion, and adhesion and inflammatory factors upregulation in HUVECs, but miR-134-5p reversed this effect.</p> Conclusion <p>GAS5 levels are decreased in DVT patients, serving as a diagnostic and prognostic biomarker. Elevated GAS5 targets miR-134-5p/FOXP3 axis to alleviate endothelial dysfunction and inflammation, thereby reducing thrombosis.</p>

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Clinical significance of lncRNA GAS5 in deep vein thrombosis and its mechanism of action on vascular endothelial damage

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月16日

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  • Hongyu Yang,
  • Shuping Wang,
  • Fei Wang

摘要

Background

The current research aims to clarify the clinical significance and molecular function of long-non-coding RNA growth arrest-specific 5 (GAS5) in deep vein thrombosis (DVT).

Methods

92 DVT patients and 86 controls were included in this study. Real-time quantitative reverse transcription PCR (RT-qPCR) was performed to measure GAS5, microRNA (miR)-134-5p, and forkhead box protein 3 (FOXP3) levels. Receiver operating characteristic (ROC) curves evaluated the diagnostic significance of GAS5 in DVT. Kaplan-Meier and Cox regression analyses assessed the prognostic significance of post-thrombotic syndrome (PTS). An in vitro model using CoCl2-induced HUVECs was established to measure cell proliferation, apoptosis, adhesion factors, and inflammatory factors via Cell Counting Kit-8 (CCK-8), flow cytometry, RT-qPCR, and Enzyme-linked immunosorbent assay (ELISA). Protein expression of FOXP3, HIF-1α, and VEGFA was evaluated via Western blot. Dual luciferase report, RIP, and RNA pull-down assays confirmed the direct binding of miR-134-5p to GAS5 or FOXP3.

Results

GAS5 and FOXP3 were downregulated in DVT patients’ serum and CoCl2-induced HUVECs, while miR-134-5p was upregulated. GAS5 distinguished DVT patients from controls with 89.13% sensitivity and 83.72% specificity. At 18-month follow-up, 32.60% of patients developed PTS, which was more common among those with low GAS5 expression. Mechanistically, GAS5 and FOXP3 bind to miR-134-5p. CoCl2 enhanced the protein levels of HIF-1α and VEGFA. Higher GAS5 levels reduced CoCl2-induced proliferation suppression, apoptosis promotion, and adhesion and inflammatory factors upregulation in HUVECs, but miR-134-5p reversed this effect.

Conclusion

GAS5 levels are decreased in DVT patients, serving as a diagnostic and prognostic biomarker. Elevated GAS5 targets miR-134-5p/FOXP3 axis to alleviate endothelial dysfunction and inflammation, thereby reducing thrombosis.