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


avatar Anna Sioziou 1 , avatar Hector Katifelis 1 , avatar Evangelia Legaki 1 , avatar Nikolaos Patelis 2 , avatar Dimitrios Athanasiadis 2 , avatar Theodoros Liakakos 2 , avatar Christos Klonaris 2 , avatar Maria Gazouli 1 , *

Department of Basic Medical Sciences, Laboratory of Biology, Medical School, National and Kapodistrian University of Athens, Athens, Greece
First Department of Surgery, Vascular Unit, National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece

how to cite: Sioziou A, Katifelis H, Legaki E, Patelis N , Athanasiadis D, et al. Expression of miR21, miR122, miR146a and miR196 in Symptomatic Carotid Disease. Int Cardiovasc Res J. 2018;12(1):e62057. 


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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