Korean Circ J.
2025 May;55(5):440-455. 10.4070/kcj.2024.0153.
LncRNA uc003pxg.1 Interacts With miR-339-5p Promote Vascular Endothelial Cell Proliferation, Migration and Angiogenesis
- Affiliations
-
- 1Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, P. R. China
- 2Department of Central Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, P. R. China
- 3Department of Pharmacy, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, P. R. China
- 4The First School of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, P. R. China
- KMID: 2568770
- DOI: http://doi.org/10.4070/kcj.2024.0153
Abstract
- Background and Objectives
This study aimed to investigate the roles of lncRNA uc003pxg.1 and miR-339-5p in regulating the occurrence and development of coronary heart disease.
Methods
First, 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 transcriptionquantitative 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.
Results
The 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.
Conclusions
Our 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.
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- RBM15-Mediated m6A Modification Regulates Proliferation and Migration of Pancreatic Cancer Cells via the lncRNA LINC01320/miR-1287-5p/FBXO11 Axis
- MSCs-Derived miR-150-5p-Expressing Exosomes Promote Skin Wound Healing by Activating PI3K/AKT Pathway through PTEN
- Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/ SOCS1 Axis
- Prolactin Inhibits BCL6 Expression in Breast Cancer Cells through a MicroRNA-339-5p-Dependent Pathway
- miR-450a-5p Eliminates MGO-Induced Insulin Resistance via Targeting CREB
