MKL1-184C&gt;T gene polymorphism is associated with coronary artery disease in the Chinese Han population

Xu, Yunzhao; Li, B.; Bao, Yinna; Zhang, X.-Y.; Zhu, Zhongyu; Zhao, Xin; Shi, Yu-Zhong; Li, D.; Chen, S.-H.; Guo, Yuexin; Cui, Chao-wei

doi:10.4238/2014.january.28.4

Cited by 2 publications

(3 citation statements)

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“…This is consistent with a previous study, and they also found that the ‐ 184C > T polymorphism of MKL1 is an important risk factor for CHD in Han nationality of Henan Province. The homozygosity of T allele is related to the risk of CHD and the severity of stenosis 25 …”

Section: Discussionmentioning

confidence: 99%

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ICAM‐1 and MKL‐1 polymorphisms impose considerable impacts on coronary heart disease occurrence

Huang

2020

J Cellular Molecular Medi

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This study was aimed to explore the correlation of intercellular adhesion molecule‐1 (ICAM‐1) K469E and megakaryoblastic leukaemia factor‐1 (MKL‐1) −184C/T polymorphisms with the susceptibility to coronary heart disease (CHD) in the Chinese Han population. 100 CHD patients and 91 healthy people that had no blood connection with each other were enrolled in this case‐control study. ICAM‐1 and MKL‐1 polymorphisms were genotyped by polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) approach. Multiple logistic regression was used to analyse the correlation between polymorphisms of ICAM‐1 and MKL‐1 and CHD susceptibility. Differences of genotype and allele frequencies of the two SNPs between case and control groups were analysed by chi‐square test. Odds ratios (ORs) and 95% confidence intervals (CIs) were indicated relative susceptibility of CHD. The distributions of ICAM‐1 and MKL‐1 polymorphisms in each group conformed to Hardy‐Weinberg equilibrium (HWE). After adjusting for traditional risk factors, the TT genotype frequency of MKL‐1 −184C/T polymorphism was found significantly higher in case group than in control group (P < .05). Meanwhile, T allele frequency increased in case group compared with control group, and the differences had statistical significance (P = .04, OR = 2.34, 95% CI = 1.34‐5.26). Logistic regression analysis in this study proved that smoking, hypertension, diabetes and triglyceride (TG) were all risk factors for CHD ICAM‐1 K469E polymorphism has no association with the onset of CHD. But MKL‐1 −184C/T polymorphism is associated with the risk of CHD and T allele might be a susceptibility factor for CHD.

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Section: Discussionmentioning

confidence: 99%

“…The homozygosity of T allele is related to the risk of CHD and the severity of stenosis. 25 Many researches on the relationship between ICAM-1 polymorphisms and inflammatory diseases have been reported. 26,27 Correlation analyses on ICAM-1 K469E polymorphism and CHD have been reported…”

Section: Discussionmentioning

confidence: 99%

ICAM‐1 and MKL‐1 polymorphisms impose considerable impacts on coronary heart disease occurrence

Huang

2020

J Cellular Molecular Medi

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“…Minami et al have demonstrated that MRTF-A deficiency in an Apoe −/− background retards the process of atherosclerosis in mice [ 17 ]. Besides, population studies have identified a position correlation between MRTF-A polymorphisms and increased risk of coronary heart disease [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

SIRT6 mediates MRTF-A deacetylation in vascular endothelial cells to antagonize oxLDL-induced ICAM-1 transcription

et al. 2022

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Oxidized low-density lipoprotein (oxLDL), a known risk factor for atherosclerosis, activates the transcription of adhesion molecules (ICAM-1) in endothelial cells. We previously showed that myocardin-related transcription factor A (MRTF-A) mediates oxLDL-induced ICAM-1 transcription. Here we confirm that ICAM-1 transactivation paralleled dynamic alterations in MRTF-A acetylation. Since treatment with the antioxidant NAC dampened MRTF-A acetylation, MRTF-A acetylation appeared to be sensitive to cellular redox status. Of interest, silencing of SIRT6, a lysine deacetylase, restored MRTF-A acetylation despite the addition of NAC. SIRT6 directly interacted with MRTF-A to modulate MRTF-A acetylation. Deacetylation of MRTF-A by SIRT6 led to its nuclear expulsion thus dampening MRTF-A occupancy on the ICAM-1 promoter. Moreover, SIRT6 expression was downregulated with oxLDL stimulation likely owing to promoter hypermethylation in endothelial cells. DNA methyltransferase 1 (DNMT1) was recruited to the SIRT6 promoter and mediated SIRT6 repression. The ability of DNMT1 to repress SIRT6 promoter partly was dependent on ROS-sensitive serine 154 phosphorylation. In conclusion, our data unveil a novel DNMT1-SIRT6 axis that contributes to the regulation of MRTF-A acetylation and ICAM-1 transactivation in endothelial cells.

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MKL1-184C>T gene polymorphism is associated with coronary artery disease in the Chinese Han population

Cited by 2 publications

References 20 publications

ICAM‐1 and MKL‐1 polymorphisms impose considerable impacts on coronary heart disease occurrence

ICAM‐1 and MKL‐1 polymorphisms impose considerable impacts on coronary heart disease occurrence

SIRT6 mediates MRTF-A deacetylation in vascular endothelial cells to antagonize oxLDL-induced ICAM-1 transcription

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