Expression of miR21, miR122, miR146a and miR196 in Symptomatic Carotid Disease

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Sioziou Anna; Katifelis Hector; Legaki Evangelia; Patelis Nikolaos; Athanasiadis Dimitrios; Liakakos Theodoros; Klonaris Christos; Gazouli Maria

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Journal: INTERNATIONAL CARDIOVASCULAR RESEARCH JOURNAL Year:2018 | Volume:12 | Issue:1 Page(s): 7-12

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Title

Expression of miR21, miR122, miR146a and miR196 in Symptomatic Carotid Disease

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Keywords

Carotid Artery Diseases MicroRNAs Inflammation

Abstract

Background: Carotid disease is one of the many forms of cardiovascular disease, which may lead to chronic disability and death. It is a multifactorial inflammatory disease, greatly affected by an individual’ s habits like smoking, lack of exercise, and a diet high in fats. MicroRNAs (miRs) are known to be involved in vascular inflammation. Objectives: We aimed to analyse in a case-control study the expression profile of selected miRs from patients with symptomatic carotid disease and to examine their involvement in the disease pathogenesis. Patients and Methods: Samples from 38 symptomatic patients who underwent carotid endarterectomy were collected and adjacent healthy regions from 15 patients were used as control samples. Fold change in the expression of miR21, miR122, miR146a and miR196α was measured using reverse transcription-real time PCR. Western blot was used to quantify the levels of MMP2 protein whose gene is a target of miR21. Results: Compared to control samples, all patients showed upregulation of miR21, miR122, miR146a and miR196a. No statistical significance was found to exist from patients with high or low miRs expression and clinical/laboratory parameters. The levels of MMP2 were found to be decreased in patients when compared to control samples. Conclusions: Our results revealed miRs which showed different expression in endarterectomy specimens from patients with symptomatic carotid disease, suggesting that these miRs correlated with vascular inflammation. Furthermore, mir21 seems an appealing pharmaceutical target since by targeting MMP2 can favour a stable plaque since low levels of the protein of its gene MMP2 target prevent the fibrous cap of the atheroma from getting thinner. Thus, miR21 seems to prevent rupture but further research is required.

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APA: Copy

Sioziou, Anna, Katifelis, Hector, Legaki, Evangelia, Patelis, Nikolaos, Athanasiadis, Dimitrios, Liakakos, Theodoros, Klonaris, Christos, & Gazouli, Maria. (2018). Expression of miR21, miR122, miR146a and miR196 in Symptomatic Carotid Disease. INTERNATIONAL CARDIOVASCULAR RESEARCH JOURNAL, 12(1), 7-12. SID. https://sid.ir/paper/767525/en

Vancouver: Copy

Sioziou Anna, Katifelis Hector, Legaki Evangelia, Patelis Nikolaos, Athanasiadis Dimitrios, Liakakos Theodoros, Klonaris Christos, Gazouli Maria. Expression of miR21, miR122, miR146a and miR196 in Symptomatic Carotid Disease. INTERNATIONAL CARDIOVASCULAR RESEARCH JOURNAL[Internet]. 2018;12(1):7-12. Available from: https://sid.ir/paper/767525/en

IEEE: Copy

Anna Sioziou, Hector Katifelis, Evangelia Legaki, Nikolaos Patelis, Dimitrios Athanasiadis, Theodoros Liakakos, Christos Klonaris, and Maria Gazouli, “Expression of miR21, miR122, miR146a and miR196 in Symptomatic Carotid Disease,” INTERNATIONAL CARDIOVASCULAR RESEARCH JOURNAL, vol. 12, no. 1, pp. 7–12, 2018, [Online]. Available: https://sid.ir/paper/767525/en

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