Simvastatin-enhanced expression of promyogenic nuclear factors and cardiomyogenesis of murine embryonic stem cells

Yang, Chen Die; Madonna, Rosalinda; Li, Yangxin; Zhang, Qi; Shen, Wei Feng; McNamara, Katharine; Yang, Yue; Geng, Yong

doi:10.1016/j.vph.2013.10.004

Cited by 5 publications

(7 citation statements)

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“…However, Yang et al . reported that simvastatin, another statin, increased myocardin expression in embryomic stem cells . Stretch can cause smooth muscle hypertrophy, and we found that cyclic stretch increased myocardin expression to cause rat aortic smooth muscle cell hypertrophy .…”

Section: Use Of Atorvastatin To Inhibit Hypoxia‐induced Myocardin Expsupporting

confidence: 52%

“…These findings reinforce our statement that cardiomyocyte hypertrophy can be prevented by suppression of myocardin expression. However, Yang et al reported that simvastatin, another statin, increased myocardin expression in embryomic stem cells [54]. Stretch can cause smooth muscle hypertrophy, and we found that cyclic stretch increased myocardin expression to cause rat aortic smooth muscle cell hypertrophy [55].…”

Section: Use Of Atorvastatin To Inhibit Hypoxia-induced Myocardin Expmentioning

confidence: 54%

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Research update for articles published in EJCI in 2012

Dullaart

Al-Daghri

Ashina

et al. 2014

Eur J Clin Investigation

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Section: Use Of Atorvastatin To Inhibit Hypoxia‐induced Myocardin Expsupporting

confidence: 52%

Section: Use Of Atorvastatin To Inhibit Hypoxia-induced Myocardin Expmentioning

confidence: 54%

Research update for articles published in EJCI in 2012

Dullaart

Al-Daghri

Ashina

et al. 2014

Eur J Clin Investigation

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“…mESCs were maintained on gelatin-coated plates in feeder-free Iscove's modified Dulbecco's medium (IMDM) (Invitrogen) supplemented with 10% fetal bovine serum (FBS) (ES qualified, Invitrogen), 1% nonessential amino acids, 1% penicillin-streptomycin, 4.5 × 10 −4 M α-monothioglycerol (α-MTG; Sigma), 1,000 U/mL leukemia inhibitory factor (LIF). Cardiac differentiation of mESCs was performed as previously described ( Yang et al., 2014 ). In brief, mESCs were developed into EBs (1,250 cells/drop) in a 3D hanging-drop culture for 4 days with LIF-free differentiation medium (IMDM supplemented with 10% FBS, 1% nonessential amino acids, 1% penicillin-streptomycin, and 4.5 × 10 −4 M α-MTG).…”

Section: Methodsmentioning

confidence: 99%

“…Deletion or mutation of these genes can lead to CHDs. Moreover, our previous work has demonstrated that expression of certain cardiac transcription factors is critical for the differentiation of embryonic stem cells (ESCs) into cardiac lineages ( Madonna et al., 2008 , Yang et al., 2014 ). However, little is known about the impact of nicotine on the expression of cardiac transcription factors.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Gata4 and Tbx5 by Nicotine-Mediated DNA Methylation in Myocardial Differentiation

Jiang

Yuan

et al. 2017

Stem Cell Reports

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SummaryMaternal nicotine exposure causes alteration of gene expression and cardiovascular programming. The discovery of nicotine-medicated regulation in cardiogenesis is of major importance for the study of cardiac defects. The present study investigated the effect of nicotine on cardiac gene expression and epigenetic regulation during myocardial differentiation. Persistent nicotine exposure selectively inhibited expression of two cardiac genes, Tbx5 and Gata4, by promoter DNA hypermethylation. The nicotine-induced suppression on cardiac differentiation was restored by general nicotinic acetylcholine receptor inhibition. Consistent results of Tbx5 and Gata4 gene suppression and cardiac function impairment with decreased left ventricular ejection fraction were obtained from in vivo studies in offspring. Our results present a direct repressive effect of nicotine on myocardial differentiation by regulating cardiac gene suppression via promoter DNA hypermethylation, contributing to the etiology of smoking-associated cardiac defects.

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“…12 Interestingly, our previous study has shown that treatment with statins promotes the cardiomyogenesis of stem cells via inducing expression of promyogenic genes. 13 Therefore, we have pursued a clinical study to translate the preclinical research into the combined application of intensive statin and MNCs in patients with ST-elevated myocardial infarction (STEMI) to offer a novel strategy for improving the postinfarct cardiac microenvironment and augmenting the efficacy of MNC transplantation in AMI patients.…”

Section: How Might This Impact On Clinical Practice?mentioning

confidence: 99%

Strengthening effects of bone marrow mononuclear cells with intensive atorvastatin in acute myocardial infarction

et al. 2020

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ObjectiveTo test whether intensive atorvastatin (ATV) increases the efficacy of transplantation with autologous bone marrow mononuclear cells (MNCs) in patients suffering from anterior ST-elevated myocardial infarction (STEMI).MethodsThis clinical trial was under a 2×2 factorial design, enrolling 100 STEMI patients, randomly into four groups of regular (RA) or intensive ATV (IA) with MNCs or placebo. The primary endpoint was the change of left ventricular ejection fraction (LVEF) at 1-year follow-up from baseline, primarily assessed by MRI. The secondary endpoints included other parameters of cardiac function, remodelling and regeneration determined by MRI, echocardiography, positron emission tomography (PET) and biomarkers.ResultsAll the STEMI patients with transplantation of MNCs showed significantly increased LVEF change values than those with placebo (p=0.01) with only in the IA+MNCs patients group demonstrating significantly elevation of LVEF than in the IA+placebo group (+12.6% (95%CI 10.4 to 19.3) vs +5.0% (95%CI 4.0 to 10.0), p=0.001), pointing to a better synergy between ATV and MNCs (p=0.019). PET analysis revealed significantly increased viable areas of myocardium (p=0.015), while the scar sizes (p=0.026) and blood aminoterminal pro-B-type natriuretic peptide (p<0.034) reduced. All these above benefits of MNCs were also attributed to IA+MNCs instead of RA+MNCs group of patients with STEMI.ConclusionsIntensive ATV treatment augments the therapeutic efficacy of MNCs in patients with anterior STEMI at the convalescent stage. The treatment with the protocol of intensive ATV and MNC combination offers a clinically essential approach for myocardial infarction.Trial registration numberNCT00979758.

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Simvastatin-enhanced expression of promyogenic nuclear factors and cardiomyogenesis of murine embryonic stem cells

Cited by 5 publications

References 50 publications

Research update for articles published in EJCI in 2012

Research update for articles published in EJCI in 2012

Inhibition of Gata4 and Tbx5 by Nicotine-Mediated DNA Methylation in Myocardial Differentiation

Strengthening effects of bone marrow mononuclear cells with intensive atorvastatin in acute myocardial infarction

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