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Updated: Jun 18, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncRNA HCG18 affects aortic dissection through the miR-103a-3p/HMGA2 axis by modulating proliferation and apoptosis
ZhiHong Yang1, YuanSheng Cui1, ShuGuo Xu1
1Department of Invasive Technology, Ningde Municipal Hospital of Ningde Normal University, Ningde City, Fujian Province, China.
Insights
Long non-coding RNA HCG18 aggravates aortic dissection (AD) by promoting Vascular Smoothing Muscle Cell proliferation and inhibiting apoptosis via the miR-103a-3p/HMGA2 pathway. Targeting HCG18 may offer a therapeutic strategy for AD.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Vascular Pathology
Background:
- Aortic dissection (AD) is a life-threatening vascular condition with limited therapeutic options.
- Understanding the molecular mechanisms underlying AD is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role and regulatory mechanism of long non-coding RNA (lncRNA) HCG18 in the pathogenesis of AD.
- To elucidate the interaction between HCG18, miR-103a-3p, and HMGA2 in AD progression.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to measure HCG18, miR-103a-3p, and HMGA2 levels in AD patient tissues.
- In vitro assays (CCK-8, colony formation, Western blot, flow cytometry) to assess VSMC proliferation and apoptosis.
- Bioinformatic analysis and dual-luciferase reporter assays to confirm targeting relationships.
- In vivo studies using a rat model of AD.
Main Results:
- HCG18 and HMGA2 were upregulated, while miR-103a-3p was downregulated in aortic tissues of AD patients.
- Downregulation of HCG18 or upregulation of miR-103a-3p promoted VSMC proliferation and reduced apoptosis.
- HCG18 acts as a competing endogenous RNA, sponging miR-103a-3p to upregulate HMGA2, thereby influencing VSMC behavior.
- HCG18 downregulation ameliorated aortic pathological injury in an AD rat model.
Conclusions:
- HCG18 exacerbates AD by promoting VSMC proliferation and inducing apoptosis through the miR-103a-3p/HMGA2 axis.
- The HCG18/miR-103a-3p/HMGA2 pathway represents a potential therapeutic target for managing AD.
Background:
Aortic Dissection (AD) is a vascular disease with a high mortality rate and limited treatment strategies. The current research analyzed the function and regulatory mechanism of lncRNA HCG18 in AD.
Methods:
HCG18, miR-103a-3p, and HMGA2 levels in the aortic tissue of AD patients were examined by RT-qPCR. After transfection with relevant plasmids, the proliferation of rat aortic Vascular Smoothing Muscle Cells (VSMCs) was detected by CCK-8 and colony formation assay, Bcl-2 and Bax was measured by Western blot, and apoptosis was checked by flow cytometry. Then, the targeting relationship between miR-103a-3p and HCG18 or HMGA2 was verified by bioinformation website analysis and dual luciferase reporter assay. Finally, the effect of HCG18 was verified in an AD rat model induced by β-aminopropionitrile.
Results:
HCG18 and HMGA2 were upregulated and miR-103a-3p was downregulated in the aortic tissues of AD patients. Downregulating HCG18 or upregulating miR-103a-3p enhanced the proliferation of VSMCs and limited cell apoptosis. HCG18 promoted HMGA2 expression by competing with miR-103a-3p and restoring HMGA2 could impair the effect of HCG18 downregulation or miR-103a-3p upregulation in mediating the proliferation and apoptosis of VSMCs. In addition, down-regulation of HCG18 could improve the pathological injury of the aorta in AD rats.
Conclusion:
HCG18 reduces proliferation and induces apoptosis of VSMCs through the miR-103a-3p/HMGA2 axis, thus aggravating AD.
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