scholarly journals Analysis of MicroRNAs Associated With Carotid Atherosclerotic Plaque Rupture With Thrombosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Peng Nie ◽  
Fan Yang ◽  
Fang Wan ◽  
Shuxuan Jin ◽  
Jun Pu
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Vascular Wall ◽  
Intraplaque Hemorrhage ◽  
Control Group ◽  
Left Carotid Artery ◽  
Mirna Microarray ◽  
Post Surgery ◽  
Atherosclerotic Plaque Rupture

Atherosclerosis is a progressive vascular wall inflammatory disease, and the rupture of atherosclerotic vulnerable plaques is the leading cause of morbidity and mortality worldwide. This study intended to explore the potential mechanisms behind plaque rupture and thrombosis in ApoE knockout mice. The spontaneous plaque rupture models were established, and left carotid artery tissues at different time points (1-, 2-, 4-, 6-, 8-, 12-, and 16-week post-surgery) were collected. By the extent of plaque rupture, plaque was defined as (1) control groups, (2) atherosclerotic plaque group, and (3) plaque rupture group. Macrophage (CD68), MMP-8, and MMP-13 activities were measured by immunofluorescence. Cytokines and inflammatory markers were measured by ELISA. The left carotid artery sample tissue was collected to evaluate the miRNAs expression level by miRNA-microarray. Bioinformatic analyses were conducted at three levels: (2) vs. (1), (3) vs. (2), and again in seven time series analysis. The plaque rupture with thrombus and intraplaque hemorrhage results peaked at 8 weeks and decreased thereafter. Similar trends were seen in the number of plaque macrophages and lipids, the expression of matrix metalloproteinase, and the atherosclerotic and plasma cytokine levels. MiRNA-microarray showed that miR-322-5p and miR-206-3p were specifically upregulated in the atherosclerotic plaque group compared with those in the control group. Meanwhile, miR-466h-5p was specifically upregulated in the plaque rupture group compared with the atherosclerotic plaque group. The highest incidence of plaque rupture and thrombosis occurred at 8 weeks post-surgery. miR-322-5p and miR-206-3p may be associated with the formation of atherosclerotic plaques. miR-466h-5p may promote atherosclerotic plaque rupture via apoptosis-related pathways.

scholarly journals Atherosclerotic plaque rupture and intraplaque hemorrhage do not correlate with symptoms in carotid artery stenosis

2003 ◽  
Vol 38 (6) ◽  
pp. 1241-1247 ◽  
Author(s):  
José Milei ◽  
Juan C Parodi ◽  
Mariano Ferreira ◽  
Andrea Barrone ◽  
Daniel R Grana ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Carotid Artery Stenosis ◽  
Plaque Rupture ◽  
Artery Stenosis ◽  
Intraplaque Hemorrhage ◽  
Atherosclerotic Plaque Rupture

scholarly journals Atherosclerotic plaque rupture in symptomatic carotid artery stenosis

1996 ◽  
Vol 23 (5) ◽  
pp. 755-766 ◽  
Author(s):  
Sandra Carr ◽  
Andrew Farb ◽  
William H. Pearce ◽  
Renu Virmani ◽  
James S.T. Yao
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Carotid Artery Stenosis ◽  
Plaque Rupture ◽  
Artery Stenosis ◽  
Symptomatic Carotid ◽  
Atherosclerotic Plaque Rupture

Ferrite-encapsulated nanoparticles with stable photothermal performance for multimodal imaging-guided atherosclerotic plaque neovascularization therapy

2021 ◽  
Author(s):  
Zhuowen Yang ◽  
Jianting Yao ◽  
Jianxin Wang ◽  
Cong Zhang ◽  
Yang Cao ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Multimodal Imaging ◽  
Plaque Rupture ◽  
Pathological Angiogenesis ◽  
Atherosclerotic Plaque Rupture ◽  
Encapsulated Nanoparticles

Pathological angiogenesis is a critical contributor to atherosclerotic plaque rupture. However, there are few effective theranostic strategies to stabilize plaques by suppressing neovascularization. A polymeric nanosystem using 3 nm manganese...

scholarly journals Applicability of Recent Dyslipidemia Guidelines in Clinical Practice

2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 43
Author(s):  
Erwinanto Erwinanto
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Coronary Flow ◽  
Cardiovascular Events ◽  
Ldl Cholesterol ◽  
Plaque Rupture ◽  
Heart Association ◽  
Plaque Stabilization ◽  
Plaque Regression ◽  
Atherosclerotic Plaque Rupture

Atherosclerotic plaque rupture is closely related to acute coronary syndromes.Stabilization of atherosclerotic plaque which slashes plaque rupture is as importantas regression ofplaque size for reducing cardiovascular events. Dyslipidemia therapy targeting to decrease LDL cholesterol reduces cardiovascular events such as acute myocard infarct, stroke, and death which are suggested to be the result of plaque stabilization. Dyslipidemia therapy also regress atherosclerotic plaque into a smaller volume. Plaque regression improves coronary flow responsible for the reduction of myocardial infarction incidence in patients with coronary heart disease (CHD).This paper consists of two parts. The first part discusses the evidence of cardiovascular event reduction with statin. The second part describes dyslipidemia management based on the 2017 Indonesian Heart Association (PERKI) Guideline on the Management of Dyslipidemia

Abstract 13: Inhibition of Nudt6 Stabilizes Advanced Atherosclerotic Plaques

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Hong Jin ◽  
Yuhuang Li ◽  
Ekaterina Chernogubova ◽  
Alexandra Bäcklund ◽  
Stina Sellberg ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Survival Rates ◽  
Atherosclerotic Plaques ◽  
Protein Coding ◽  
Fibrous Cap ◽  
Asymptomatic Patients ◽  
Rupture Model

Natural antisense transcripts (NATs), a non-coding RNA subclass, being transcribed in antisense direction to protein coding genes, are an intriguing novel class of targetable modulators, exerting crucial effects on gene expression. Aim of the current study was to investigate the contribution of NATs to atherosclerotic plaque vulnerability. Using laser capture micro-dissection, we isolated fibrous caps tissue of carotid artery plaques from 20 symptomatic patients with ruptured lesions vs. 20 samples from asymptomatic patients with stable lesions. A human transcriptome array (HTA; GeneChip 2.0 ) was used to profile the expression of all currently annotated RNA transcripts. Nucleoside diphosphate-linked moiety X motif 6 (NUDT6) was identified as one of the most significantly up-regulated transcripts in fibrous caps of ruptured lesions. Interestingly, NUDT6 is an established antisense RNA targeting the fibroblast growth factor 2 (FGF2). Of importance, FGF2 was among the most significantly down-regulated transcripts in ruptured lesions, corresponding to elevated NUDT6 expression. In situ hybridization in both, human and mouse carotid atherosclerotic plaques, confirmed substantially higher expression levels of NUDT6 in ruptured lesions compared to stable. In addition, in situ hybridization revealed a distinct co-localization with smooth muscle cells (SMCs) in advanced plaques. Overexpression of NUDT6 in cultured human carotid artery SMCs effectively limited FGF2 on the mRNA as well as protein level. Furthermore, reduction of NUDT6 via siRNA stimulated proliferation and blocked apoptosis in SMCs. In an inducible atherosclerotic plaque rupture model using incomplete ligation and cuff placement on common carotid arteries of male apoE -/- mice, NUDT6 inhibition with gapmeRs was able to significantly improve SMC survival rates, leading to thicker fibrous caps, and to reduce the plaque rupture rate compared to scramble-gapmeR control-treated mice (22% vs . 63%, p = 0.03). The present study presents NUDT6 as a novel crucial antisense regulator of fibrous cap stability through steering SMC survival via targeting its sense RNA transcript FGF2.

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