LncRNA PARD3-AS1 regulates the proliferation and migration of human umbilical vein endothelial cells in atherosclerosis by targeting miR-668-3p
- 1Department of Vascular Surgery, The Affiliated Hospital of Qingdao University
- 2Department of Obstetrics and Gynecology, People’s Hospital of Zhaoyuan City
Abstract
Long non-coding RNAs (lncRNAs) play crucial roles in the onset and progression of cardiovascular disease, particularly atherosclerosis. However, the role of PARD3-AS1 in atherosclerosis remains largely uncharacterized. This study therefore aimed to investigate the impact of the PARD3-AS1/miR-668-3p axis on atherosclerosis. The expression levels of PARD3-AS1 and miR-668-3p in human umbilical vein endothelial cells (HUVECs) were quantified by quantitative real-time polymerase chain reaction (RT-qPCR). HUVEC proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and migratory and invasive capacities were evaluated using wound healing and Transwell assays. The interaction between PARD3-AS1 and miR-668-3p was confirmed by bioinformatics analysis and dual-luciferase reporter assays. In addition, serum samples were collected from patients diagnosed with atherosclerosis, and ApoE⁻/⁻ C57BL/6 mice were fed a high-fat diet for 8 weeks to establish a model of atherosclerosis. PARD3-AS1 expression was significantly reduced in the serum of patients with atherosclerosis, whereas miR-668-3p levels were markedly elevated, and the two were negatively correlated. Subsequent experiments confirmed that miR-668-3p effectively reversed the promotion effects of PARD3-AS1 on HUVEC proliferation and migration. In vivo, histological staining showed that the PARD3-AS1 overexpression group exhibited improved endothelial repair. Collectively, these findings demonstrate that PARD3-AS1 directly interacts with miR-668-3p to modulate HUVEC proliferation, migration, and invasion, suggesting that PARD3-AS1 may serve as a potential therapeutic target for atherosclerosis.
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BibTeX
@article{sun2026lncrna,
title = {{LncRNA PARD3-AS1 regulates the proliferation and migration of human umbilical vein endothelial cells in atherosclerosis by targeting miR-668-3p}},
author = {Xiaozhi Sun and Linlin Zhang and Xinxing Wang and Junwei Yan and Xuefei Jiao and Yongxin Li and Mingjin Guo},
journal = {Scientific Reports},
year = {2026},
month = jul,
doi = {10.1038/s41598-026-62404-7},
url = {https://doi.org/10.1038/s41598-026-62404-7},
note = {CC BY},
}
RIS
TY - JOUR
TI - LncRNA PARD3-AS1 regulates the proliferation and migration of human umbilical vein endothelial cells in atherosclerosis by targeting miR-668-3p
AU - Xiaozhi Sun
AU - Linlin Zhang
AU - Xinxing Wang
AU - Junwei Yan
AU - Xuefei Jiao
AU - Yongxin Li
AU - Mingjin Guo
PY - 2026
DA - 2026/07/01
JO - Scientific Reports
DO - 10.1038/s41598-026-62404-7
UR - https://doi.org/10.1038/s41598-026-62404-7
AB - Long non-coding RNAs (lncRNAs) play crucial roles in the onset and progression of cardiovascular disease, particularly atherosclerosis. However, the role of PARD3-AS1 in atherosclerosis remains largely uncharacterized. This study therefore aimed to investigate the impact of the PARD3-AS1/miR-668-3p axis on atherosclerosis. The expression levels of PARD3-AS1 and miR-668-3p in human umbilical vein endothelial cells (HUVECs) were quantified by quantitative real-time polymerase chain reaction (RT-qPCR). HUVEC proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and migratory and invasive capacities were evaluated using wound healing and Transwell assays. The interaction between PARD3-AS1 and miR-668-3p was confirmed by bioinformatics analysis and dual-luciferase reporter assays. In addition, serum samples were collected from patients diagnosed with atherosclerosis, and ApoE⁻/⁻ C57BL/6 mice were fed a high-fat diet for 8 weeks to establish a model of atherosclerosis. PARD3-AS1 expression was significantly reduced in the serum of patients with atherosclerosis, whereas miR-668-3p levels were markedly elevated, and the two were negatively correlated. Subsequent experiments confirmed that miR-668-3p effectively reversed the promotion effects of PARD3-AS1 on HUVEC proliferation and migration. In vivo, histological staining showed that the PARD3-AS1 overexpression group exhibited improved endothelial repair. Collectively, these findings demonstrate that PARD3-AS1 directly interacts with miR-668-3p to modulate HUVEC proliferation, migration, and invasion, suggesting that PARD3-AS1 may serve as a potential therapeutic target for atherosclerosis.
SN - 2045-2322
ER -