MicroRNA-328 as a regulator of cardiac hypertrophy

Li, Cui; Li, Xuelian; Gao, Xu; Zhang, Ruixue; Zhang, Ying; Liang, Haihai; Xu, Chaoqian; Du, Weijie; Zhang, Yong; Li, Xue; Ma, Ning; Xu, Zhidan; Wang, Leimin; Chen, Xu; Lu, Yanjie; Ju, Jiaming; Yang, Baofeng; Shan, Hongli

doi:10.1016/j.ijcard.2014.02.035

Cited by 77 publications

(75 citation statements)

References 38 publications

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“…The mice were then intubated with an endotracheal cannula connected to a volume cycled rodent ventilator with a tidal volume of 50 ml and a respiratory rate of 100 per min (UGO BASILE S. R. L., Italy). TAC was then performed in accordance with previously described methods [19]. In brief, the aortic arch was identified after thoracotomy was performed.…”

Section: In Vivo Hypertrophy Inductionmentioning

confidence: 99%

“…In brief, the aortic arch was identified after thoracotomy was performed. A 7.0-silk suture was placed around the transverse aorta between the innominate and left carotid arteries and then ligated around a 26-gauge blunt needle, which was subsequently removed; as a result, systolic pressure was increased by 1.5-fold to induce VH [19]. The sham-operated control mice underwent the same surgical procedures, but the aorta of these mice was not ligated.…”

Section: In Vivo Hypertrophy Inductionmentioning

confidence: 99%

“…Transmission electron microscopy was performed on randomly selected LV sections as previously described [19]. In brief, the selected samples (5 nm) were fixed with 2.5% glutaraldehyde in 0.1 mol$L -1 PBS (pH 7.4) for 2 h, post-fixed in PBS buffer containing 1% osmium tetraoxide (OsO 4 ) for 1 h, and embedded as a monolayer.…”

Section: Transmission Electron Microscopymentioning

confidence: 99%

“…The drug is efficacious and appropriate for rats younger than postnatal day 3 [21]. The rats were sacrificed through decapitation, and the hearts were isolated after thoracotomy was performed; the cardiac tissue was digested and then cultured in accordance with previously described methods [19,20]. In brief, heart tissue was digested in 0.25% trypsin at 37°C.…”

Section: Primary Neonatal Rat Cardiomyocyte Culturementioning

confidence: 99%

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Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Gitau

Zhao

et al. 2015

Front. Med.

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Ventricular hypertrophy is a powerful and independent predictor of cardiovascular morbid events. The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail. In this study, healthy wild-type male mice were randomly divided into three groups and subjected to transverse aortic constriction (TAC) or sham operation. The TAC-operated mice were treated with the human equivalent of low-dose aspirin (10 mg$kg); the remaining mice received an equal amount of phosphate buffered saline with 0.65% ethanol, which was used as a vehicle. A cardiomyocyte hypertrophy model induced by angiotensin II (10 nmol$L -1 ) was treated with the human equivalent of low (10 or 100 µmol$L ) aspirin concentrations in plasma. Changes in the cardiac structure and function were assessed through echocardiography and transmission electron microscopy. Gene expression was determined through RT-PCR and western blot analysis. Results indicated that aspirin treatment abrogated the increased thickness of the left ventricular anterior and posterior walls, the swelling of mitochondria, and the increased surface area in in vivo and in vitro hypertrophy models. Aspirin also normalized the upregulated hypertrophic biomarkers, β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP). Aspirin efficiently reversed the upregulation of β-catenin and P-Akt expression and the TAC-or ANG II-induced downregulation of GSK-3β. Therefore, low-dose aspirin possesses significant anti-hypertrophic properties at clinically relevant concentrations for anti-thrombotic therapy. The downregulation of β-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.

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Section: In Vivo Hypertrophy Inductionmentioning

confidence: 99%

Section: In Vivo Hypertrophy Inductionmentioning

confidence: 99%

Section: Transmission Electron Microscopymentioning

confidence: 99%

Section: Primary Neonatal Rat Cardiomyocyte Culturementioning

confidence: 99%

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Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Gitau

Zhao

et al. 2015

Front. Med.

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“…10) miR-328 has been reported to promote cardiac hypertrophy and may serve as a promising therapeutic target for this disease. 11) Recently, the crucial roles of miR-10a in the pathological process of several diseases have been attracting increasing attention. Overexpression of miR-10a contributes to the enhanced invasiveness in pancreatic cancer through suppression of the HOXA1 gene.…”

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confidence: 99%

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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SummaryThe mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy. (Int Heart J 2017; 58: 100-106)

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MicroRNA signatures differentiate preserved from reduced ejection fraction heart failure

Watson

Gupta

O’Connell

et al. 2015

European J of Heart Fail

183

143

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AimsDifferentiation of heart failure with reduced (HFrEF) or preserved (HFpEF) ejection fraction independent of echocardiography is challenging in the community. Diagnostic strategies based on monitoring circulating microRNA (miRNA) levels may prove to be of clinical value in the near future. The aim of this study was to identify a novel miRNA signature that could be a useful HF diagnostic tool and provide valuable clinical information on whether a patient has HFrEF or HFpEF.Methods and resultsMiRNA biomarker discovery was carried out on three patient cohorts, no heart failure (no-HF), HFrEF, and HFpEF, using Taqman miRNA arrays. The top five miRNA candidates were selected based on differential expression in HFpEF and HFrEF (miR-30c, −146a, −221, −328, and −375), and their expression levels were also different between HF and no-HF. These selected miRNAs were further verified and validated in an independent cohort consisting of 225 patients. The discriminative value of BNP as a HF diagnostic could be improved by use in combination with any of the miRNA candidates alone or in a panel. Combinations of two or more miRNA candidates with BNP had the ability to improve significantly predictive models to distinguish HFpEF from HFrEF compared with using BNP alone (area under the receiver operating characteristic curve >0.82).ConclusionThis study has shown for the first time that various miRNA combinations are useful biomarkers for HF, and also in the differentiation of HFpEF from HFrEF. The utility of these biomarker combinations can be altered by inclusion of natriuretic peptide. MiRNA biomarkers may support diagnostic strategies in subpopulations of patients with HF.

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MicroRNA-328 as a regulator of cardiac hypertrophy

Cited by 77 publications

References 38 publications

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

MicroRNA signatures differentiate preserved from reduced ejection fraction heart failure

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