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Published on: January 28, 2020
Correlations between vitronectin, miR-520, and miR-34 in patients with stenosis of coronary arteries
Ghasem Ghasempour1, Farhad Shaikhnia2, Ali Akbar Soleimani1
1Clinical Biochemistry Department, Faculty of Medical Sciences, Iran University of Medical Sciences, Tehran, Iran.
Insights
In-stent restenosis involves monocytes and altered expression of vitronectin, miR-34, and miR-520. Targeting vitronectin with these microRNAs may impact molecular events in vessel stenosis.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics and Proteomics
Background:
- In-stent restenosis is a complex process involving platelet activation, neointima formation, and vascular smooth muscle cell proliferation.
- Monocytes play a critical role in neointimal hyperplasia by migrating to the site of injury via chemokines and secreted proteins.
Purpose of the Study:
- To investigate the expression levels of vitronectin, miR-193, miR-34, and miR-520 in peripheral blood mononuclear cells (PBMCs) from patients with coronary artery stenosis.
- To explore the relationship between these molecular markers and the development of in-stent restenosis.
Main Methods:
- Sixty subjects were enrolled: 20 with no restenosis, 20 with in-stent restenosis, and 20 healthy controls.
- Vitronectin, miR-193, miR-34, and miR-520 expression levels were quantified using RT-qPCR.
- Statistical analysis was performed using SPSS software.
Main Results:
- Significant alterations in vitronectin, miR-34, and miR-520 expression were observed in patients with in-stent restenosis (p=0.02, p=0.02, p=0.01, respectively).
- Inverse correlations were found between vitronectin gene expression and miR-34 (r=-0.44, p=0.04) and miR-520 (r=-0.5, p=0.01).
Conclusions:
- The findings suggest that vitronectin, miR-34, and miR-520 are implicated in the molecular mechanisms of in-stent restenosis.
- Targeting vitronectin with miR-520 and miR-34 may represent a potential therapeutic strategy for vessel stenosis.
Background:
In-stent restenosis usually occurs by platelet activation, neointima formation, VSMC migration, and proliferation in the position of the vessel stent. The monocytes have a magnificent role in neointimal hyperplasia since these cells recruit to the site of vessel injury through chemokines and other secretion proteins. This study is focused on the investigation of vitronectin, miR-193, miR-34, and miR-520 expression levels in PBMCs isolated from stenosed patients.
Methods:
A total of sixty subjects undergoing coronary artery angiography containing patients with stent no restenosis (n = 20), in-stent restenosis (n = 20), and healthy participants (n = 20) participated in the study. The vitronectin, miR-193, miR-34, and miR-520 expression levels were measured by the RT-qPCR technique. Data were analyzed by SPSS software.
Results:
The vitronectin, miR-34, and miR-520 expression levels changed significantly in patients with vessel in-stent restenosis (p = 0.02, p = 0.02, and p = 0.01, respectively). Furthermore, there were inverse correlations between the expression levels of vitronectin gene and miR-34 (r = - 0.44, p = 0.04) as well as miR-520 (r = - 0.5, p=0.01).
Conclusions:
The molecular events in the vessel stenosis may be affected by targeting vitronectin with miR-520 and miR-34.
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