Tissue factor pathway inhibitor in atherosclerosis

Yuan, Hou-Qin; Yi, Hao; Zhong, Ren; Gu, Hong‐Feng; Liu, Feng-Tao; Yan, Bin-Jie; Qu, Shun-Lin; Tang, Zhi‐Han; Liu, Lu‐Shan; Chen, Da-Xing; Jiang, Zhi‐Sheng

doi:10.1016/j.cca.2019.01.024

Cited by 16 publications

(10 citation statements)

References 69 publications

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“…1 In China, the incidence of atherosclerosis is expected to increase annually, which imposed substantial medical and economic burden on the society. 2,3 To date, the pathophysiology of atherosclerosis remains unclear, and recent evidence pointed to vascular smooth muscle cells (VSMCs) as the key factor in the development of atherosclerosis. 4,5 Studies showed that abnormal VSMC proliferation, migration and synthesis of extracellular matrix by VSMCs contribute to the formation of the atherosclerotic plaque.…”

Section: Introductionmentioning

confidence: 99%

LncRNA TNK2‐AS1 regulated ox‐LDL‐stimulated HASMC proliferation and migration via modulating VEGFA and FGF1 expression by sponging miR‐150‐5p

Cai

Cui

Zhang

et al. 2019

J Cellular Molecular Medi

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Long non‐coding RNAs (lncRNAs) have been indicated for the regulatory roles in cardiovascular diseases. This study determined the expression of lncRNA TNK2 antisense RNA 1 (TNK2‐AS1) in oxidized low‐density lipoprotein (ox‐LDL)‐stimulated human aortic smooth muscle cells (HASMCs) and examined the mechanistic role of TNK2‐AS1 in the proliferation and migration of HASMCs. Our results demonstrated that ox‐LDL promoted HASMC proliferation and migration, and the enhanced proliferation and migration in ox‐LDL‐treated HASMCs were accompanied by the up‐regulation of TNK2‐AS1. In vitro functional studies showed that TNK2‐AS1 knockdown suppressed cell proliferation and migration of ox‐LDL‐stimulated HASMCs, while TNK2‐AS1 overexpression enhanced HASMC proliferation and migration. Additionally, TNK2‐AS1 inversely regulated miR‐150‐5p expression via acting as a competing endogenous RNA (ceRNA), and the enhanced effects of TNK2‐AS1 overexpression on HASMC proliferation and migration were attenuated by miR‐150‐5p overexpression. Moreover, miR‐150‐5p could target the 3’ untranslated regions of vascular endothelial growth factor A (VEGFA) and fibroblast growth factor 1 (FGF1) to regulate FGF1 and VEGFA expression in HASMCs, and the inhibitory effects of miR‐150‐5p overexpression in ox‐LDL‐stimulated HASMCs were attenuated by enforced expression of VEGFA and FGF1. Enforced expression of VEGFA and FGF1 also partially restored the suppressed cell proliferation and migration induced by TNK2‐AS1 knockdown in ox‐LDL‐stimulated HASMCs, while the enhanced effects of TNK2‐AS1 overexpression on HASMC proliferation and migration were attenuated by the knockdown of VEGFA and FGF1. Collectively, our findings showed that TNK2‐AS1 exerted its action in ox‐LDL‐stimulated HASMCs via regulating VEGFA and FGF1 expression by acting as a ceRNA for miR‐150‐5p.

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Section: Introductionmentioning

confidence: 99%

LncRNA TNK2‐AS1 regulated ox‐LDL‐stimulated HASMC proliferation and migration via modulating VEGFA and FGF1 expression by sponging miR‐150‐5p

Cai

Cui

Zhang

et al. 2019

J Cellular Molecular Medi

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“…In this study, we compared gene expression in PCAT of patients with advanced CAD and non-CAD controls. We found that (i) the top upregulated genes in CAD are involved in inflammation and atherosclerosis, 14–17 (ii) the top downregulated genes are responsible for cardiac ischaemia and remodelling, 29 , 30 platelet function, 31 , 32 mitochondrial function, 33 obesity, 34 and encode different types of collagen, and (iii) the top upstream regulators related with DEGs include molecules that have proinflammatory and atherosclerotic profile (HMGB2, PDGF and ECSIT). We identified one activated pathway related with DEGs, associated with coagulation system, and two inhibited pathways related with DEGs, associated with senescence and intrinsic prothrombin activation pathway.…”

Section: Discussionmentioning

confidence: 93%

“…The top downregulated genes included those responsible for cardiac ischaemia and remodelling (miR-3671, miR-4524a), 29 , 30 platelet function (multimerin, TFPI), 31 , 32 mitochondrial function (glucuronidases), 33 obesity (miR-548), 34 and encode different types of collagens (type I, III, IV). In line with our finding, other authors also found specific miRNA and gene signatures of EAT in CAD, with down-regulation of genes involved in mitochondrial function, lipid metabolism, nuclear receptor transcriptional activity, and up-regulation of those involved in chemokine signalling and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Atherosclerosis Pathways are Activated in Pericoronary Adipose Tissue of Patients with Coronary Artery Disease

Konwerski¹,

Gromadka²,

Arendarczyk³

et al. 2021

JIR

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“…Все это впоследствии приводит к активации тромбина и формированию тромба. Таким образом, активация внешнего пути свертывания крови играет важнейшую роль в эндотелиальной дисфункции и развитии атеросклероза [9,10]. Когортные исследования, например, исследование Martinelli N, et al, сообщают о том, что плазменная концентрация FVIIa-тканевого фактора является маркером риска общей и сердечно-сосудистой смертности у пациентов с клинически стабильной ИБС [11].…”

Section: таблица 1 частоты генотипов и аллелей однонуклеотидных полимunclassified

Polymorphisms in F2, F7, and PAI1 genes in men with coronary atherosclerosis

et al. 2020

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Aim. To study the associations of polymorphisms in F2, F7, and PAI1 genes with the presence of vulnerable plaque in coronary arteries (CA) and the blood concentration of proteins encoded by these genes.Material and methods. The study included 101 men 40-70 years old with documented coronary atherosclerosis, who underwent coronary artery bypass grafting. According to the histological analysis of atherosclerotic plaques, men were divided into 2 groups: 40 men (39,6%) with stable plaque; 61 men (60,4%) with vulnerable plaques in CA. Genotyping of rs1799963 and rs6046 was performed by reverse transcription polymerase chain reaction, rs1799889 — by polymerase chain reaction. Statistical processing was performed using the SPSS 16.0 software package.Results. In patients with stable plaques, allele A of rs6046 polymorphism in the F7 gene was observed in 2,9 times more often (95% confidence interval (CI), 1,20-7,20, p=0,021) than in men with vulnerable plaques. The odds ratio of the GA genotype carriage is 4,03 times higher among patients with stable plaques in CA compared with vulnerable plaques (95% CI, 1,49-10,93, p=0,006). The odds ratio of the 5G/4G genotype carriage among patients with stable plaques in CA is 2,47 times higher than in patients with vulnerable plaques (95% CI, 1,08-5,62, p=0,039). The 4G/4G genotype carriage is 5,85 times much more common in men with stable plaques (95% CI, 1,61-21,34, p=0,003).Conclusion. Polymorphism in the PAI1 (rs1799889) and F7 (rs6046) genes are associated with the presence of vulnerable plaques in CA in men with verified coronary atherosclerosis. There were no differences between the groups in the frequencies of genotypes and alleles of the rs1799963 polymorphism of the F2 gene. Also, no significant differences were found in the blood levels of PAI-1 and factor VII in groups with different genotypes.

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Tissue factor pathway inhibitor in atherosclerosis

Cited by 16 publications

References 69 publications

LncRNA TNK2‐AS1 regulated ox‐LDL‐stimulated HASMC proliferation and migration via modulating VEGFA and FGF1 expression by sponging miR‐150‐5p

LncRNA TNK2‐AS1 regulated ox‐LDL‐stimulated HASMC proliferation and migration via modulating VEGFA and FGF1 expression by sponging miR‐150‐5p

Atherosclerosis Pathways are Activated in Pericoronary Adipose Tissue of Patients with Coronary Artery Disease

Polymorphisms in F2, F7, and PAI1 genes in men with coronary atherosclerosis

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