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Updated: Jul 4, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-130a-3p inhibits endothelial inflammation by regulating the expression of MAPK8 in endothelial cells
Mingming Gu1, Kun Liu1, Hui Xiong1
1Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China.
Abstract:
MicroRNA-130a-3p (miR-130a-3p) has been reported as closely related to atherosclerosis (AS). This study is to survey the effects of miR-130a-3p in endothelial cells (ECs) treated with oxidized low-density lipoprotein (ox-LDL) and explore underlying mechanisms. The proliferation and apoptosis of ox-LDL-treated HUVEC cells were determined by CCK-8, EdU, and flow cytometry assays. ELISA and Western blot analysis measured the expressions of cytokines and protein levels. Bioinformatics and dual-luciferase reporter assay were performed to predict and confirm that Mitogen-activated protein kinase 8 (MAPK8) was a direct target of miR-130a-3p, and MAPK8 was negatively associated with miR-130a-3p. As expected, miR-130a-3p was down-regulated in ox-LDL-treated HUVEC cells, and up-regulation of miR-130a-3p promoted proliferation and inhibited apoptosis of ox-LDL-treated HUVEC cells. Furthermore, miR-130a-3p mimics suppressed the expressions of TNF-α and IL-6 and decreased the protein levels of VCAM-1, ICAM-1 and E-selectin. MAPK8 was highly expressed in ox-LDL-treated HUVEC cells, and silence of MAPK8 promoted proliferation inhibited apoptosis, suppressed inflammatory responses, and decreased the levels of VCAM-1, ICAM-1, and E-selectin, over-expression of MAPK8 partially restored the functional effects of miR-130a-3p on proliferation, inflammatory responses, and the expressions of VCAM-1, ICAM-1 and E-selectin. This study indicates that miR-130a-3p may emerge as an effective target for treating AS.
Insights
MicroRNA-130a-3p (miR-130a-3p) protects against atherosclerosis by promoting endothelial cell proliferation and reducing inflammation. Upregulating miR-130a-3p counteracts the effects of oxidized LDL, suggesting it as a therapeutic target.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cell Biology
Background:
- Atherosclerosis (AS) is a chronic inflammatory disease.
- Endothelial cell dysfunction is a key factor in AS pathogenesis.
- MicroRNAs play crucial roles in regulating cellular processes relevant to AS.
Purpose of the Study:
- To investigate the role of microRNA-130a-3p (miR-130a-3p) in endothelial cells (ECs) exposed to oxidized low-density lipoprotein (ox-LDL).
- To explore the underlying molecular mechanisms of miR-130a-3p in ox-LDL-treated ECs.
- To evaluate the therapeutic potential of miR-130a-3p in AS.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were treated with ox-LDL.
- Cell proliferation and apoptosis were assessed using CCK-8, EdU, and flow cytometry.
- Cytokine expression and protein levels were measured by ELISA and Western blot.
- Bioinformatics and dual-luciferase reporter assays identified MAPK8 as a direct target of miR-130a-3p.
Main Results:
- miR-130a-3p was downregulated in ox-LDL-treated HUVECs.
- Upregulation of miR-130a-3p promoted HUVEC proliferation and inhibited apoptosis.
- miR-130a-3p suppressed inflammatory markers (TNF-α, IL-6) and adhesion molecules (VCAM-1, ICAM-1, E-selectin).
- MAPK8 was upregulated by ox-LDL; its silencing mimicked miR-130a-3p's protective effects.
Conclusions:
- miR-130a-3p exerts protective effects on endothelial cells against ox-LDL-induced injury.
- miR-130a-3p targets MAPK8, mediating its anti-inflammatory and anti-apoptotic functions.
- miR-130a-3p represents a promising therapeutic target for atherosclerosis treatment.
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