Downregulation of Talin-1 is associated with the increased expression of miR-182-5p and miR-9-5p in coronary artery disease

被引:8
|
作者
Gholipour, Akram [1 ]
Shakerian, Farshad [2 ,3 ]
Zahedmehr, Ali [3 ]
Irani, Shiva [1 ]
Mowla, Seyed Javad [4 ]
Malakootian, Mahshid [2 ]
机构
[1] Islamic Azad Univ, Dept Biol, Sci & Res Branch, Tehran, Iran
[2] Iran Univ Med Sci, Cardiogenet Res Ctr, Rajaie Cardiovasc Med & Res Ctr, Tehran, Iran
[3] Iran Univ Med Sci, Cardiovasc Intervent Res Ctr, Rajaie Cardiovasc Med & Res Ctr, Tehran, Iran
[4] Tarbiat Modares Univ, Fac Biol Sci, Dept Mol Genet, Tehran, Iran
关键词
coronary artery disease; miR-182-5p; miR-9-5p; TLN1; gene; CIRCULATING MICRORNAS; ATHEROSCLEROTIC PLAQUE; EXTRACELLULAR-MATRIX; BIOMARKERS; IDENTIFICATION; INHIBITION; MECHANISMS; MONOCYTES; APOPTOSIS; VINCULIN;
D O I
10.1002/jcla.24252
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Background Evidence indicates that the dysregulation of extracellular matrix (ECM) components can lead to cardiovascular diseases. The Talin-1 (TLN1) gene is a major component of the ECM, and it mediates integrin adhesion to the ECM. In this study, we aimed to determine microRNAs (miRs) that regulate the expression of TLN1 and determine expression alterations in TLN1 and its targeting miRs in coronary artery disease (CAD). Methods Data sets of CAD and normal samples of blood exosomes were downloaded, and TLN1 was chosen as one of the genes with differential expressions in an in silico analysis. Next, miR-182-5p and miR-9-5p, which have a binding site on 3 '-UTR of TLN1, were selected using bioinformatics tools. Then, the miR target site was cloned in the psiCHECK-2 vector, and direct interaction between the miR target site and the TLN1 3 '-UTR putative target site was investigated by luciferase assay. The expression of miR-182-5p, miR-9-5p, and TLN1 in the serum samples of CAD and non-CAD individuals was assessed via a real-time quantitative polymerase chain reaction. Results Our data revealed that miR-182-5p directly regulated the expression of TLN1. Moreover, miR-182-5p and miR-9-5p were significantly upregulated in the CAD group. Hence, both bioinformatics and experimental analyses determined the downregulated expression of TLN1 in the CAD samples. Conclusions Our findings demonstrated that miR-182-5p and miR-9-5p could play significant roles in TLN1 regulation and participate in CAD development by targeting TLN1. These findings introduce novel biomarkers with a potential role in CAD pathogenesis.
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页数:9
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