Rescuing infusion of miRNA-1 prevents cardiac remodeling in a heart-selective miRNA deficient mouse

Luo, Shuilian; Chen, Yuhang; He, Rui; Shi, Yujun; Li, Su

doi:10.1016/j.bbrc.2017.11.029

Cited by 13 publications

(8 citation statements)

References 26 publications

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“…MiR-1 and miR-499 were higher in the circulation of patients with acute myocardial infarction and were suggested to have the potential to be novel, independent biomarkers for cardiac damage [ 22 , 23 ]. Luo et al found that, in a cardiac-selective miRNA-1-deficient mouse model, a decreased miR-1-expression level resulted in severe LV enlargement and remodeling [ 24 ]. The substitution of mir-1 prevented the development of cardiac hypertrophy and remodeling in these miR-1 deficient mice [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

“…Luo et al found that, in a cardiac-selective miRNA-1-deficient mouse model, a decreased miR-1-expression level resulted in severe LV enlargement and remodeling [ 24 ]. The substitution of mir-1 prevented the development of cardiac hypertrophy and remodeling in these miR-1 deficient mice [ 24 ]. Since LV hypertrophy is a hallmark of HCM patients, our results suggest that the increased level of miR-1 might also adversely affect cardiac remodeling and function.…”

Section: Discussionmentioning

confidence: 99%

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A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy

Thottakara

Lund²,

Krämer

et al. 2021

Biomolecules

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(1) Background: Left ventricular hypertrophy, myocardial disarray and interstitial fibrosis are the hallmarks of hypertrophic cardiomyopathy (HCM). Access to the myocardium for diagnostic purposes is limited. Circulating biomolecules reflecting the myocardial disease processes could improve the early detection of HCM. Circulating miRNAs have been found to reflect disease processes in several cardiovascular diseases. (2) Methods: We quantified circulating miRNA molecules in the plasma of 24 HCM and 11 healthy controls using the Human v3 miRNA Expression Assay Kit Code set (Nanostring Tech., Seattle, WA, USA) and validated differentially expressed miRNAs using RT-PCR. (3) Results: In comparison to healthy controls, the levels of six miRNAs (miR-1, miR-3144, miR-4454, miR-495-3p, miR-499a-5p and miR-627-3p) were higher in the plasma of HCM patients than healthy individuals (p < 0.05). Of these, higher levels of miR-1, miR-495 and miR-4454 could be validated by real-time PCR. In addition, elevated miR-4454 levels were significantly correlated with cardiac fibrosis, detected by magnetic resonance imaging in HCM patients. (4) Conclusions: Circulating miR-1, miR-495-3p and miR-4454 levels are elevated in the plasma of HCM patients. To the best of our knowledge, this is the first report showing a correlation between miR-4454 levels and cardiac fibrosis in HCM. This suggests miR-4454 as a potential biomarker for fibrosis in these patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy

Thottakara

Lund²,

Krämer

et al. 2021

Biomolecules

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“…A subset of miRNAs has been shown to be highly and speci cally expressed in the heart muscle, including miRNA-378, miRNA-208, miRNA-499 and miRNA-22 [38,39]. For example, it has been found that overexpression of miRNA-133a in cardiomyocytes signi cantly reduces H 2 O 2 induced cardiomyocyte apoptosis, indicating that miRNA plays a critical role in the mechanism of anti-cardiomyocyte apoptosis [40].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SUMO1P3 Aggravates Doxorubicin-Induced Cardiomyocyte Apoptosis by Targeting miR-93-5p / Bin1

Lin

2021

Preprint

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Background/AimsNon-coding RNA plays a critical role in myocardial apoptosis induced by doxorubicin (DOX). However, the specific function of Long noncoding RNA (lncRNA) small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) is unclear. The purpose of this study was to determine the role of lncRNA SUMO1P3 in myocardial apoptosis induced by DOX. MethodsQRT-PCR were used to detect the expression levels of SUMO1P3 and miR-93-5p in DOX-treated primary cardiomyocytes and rat models. QRT-PCR and Western blot were used to detect the expression levels of Bin1 in DOX-treated primary cardiomyocytes and rat models. The relationship between SUMO1P3, miR-93-5p and Bin1 was analyzed using bioinformatics analysis and Luciferase reporter assay. The effects of DOX on the viability and apoptosis of cardiomyocytes were evaluated by flow cytometry and CCK-8. The effects of SUMO1P3 on cardiomyocyte apoptosis were analyzed by TUNEL staining and echocardiography. ResultsIn DOX-treated primary cardiomyocytes and rat models, the expression levels of SUMO1P3 and Bin1 were significantly increased, while the expression levels of miR-93-5p were significantly reduced. MiR-93-5p was a direct target gene of SUMO1P3, and Bin1 was a direct target gene of miR-93-5p. In addition, miR-93-5p reversed the protective effect of SUMO1P3 knockout on cardiomyocytes by inhibiting the expression of Bin1. ConclusionSUMO1P3 inhibited DOX-induced cardiomyocyte apoptosis through miR-93-5p/Bin1 axis.

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“…These dysfunctional changes develop despite the compensatory enhanced SERCA expression and normal myocardial structure [51], emphasizing the important role of mtCU regulatory subunits and upstream regulatory molecules in the mitochondrial Ca 2+ handling under pathological conditions. For instance, miR-1 is being extensively studied as a potential therapeutic target, given its contribution to cardiac hypertrophy [72] and remodeling [126] and its association with heart failure [127], whereas mtCU has been identified as a downstream target of miR-1 in the hypertrophic changes realization [72]. Nevertheless, prognostic value of miR-1/mtCU axis in the heart failure progression has not been assessed thoroughly.…”

Section: The Role Of Mtcu In Cardiac Musclementioning

confidence: 99%

Mitochondrial Calcium Uniporter Structure and Function in Different Types of Muscle Tissues in Health and Disease

Тарасова

Vishnyakova

Logashina

et al. 2019

IJMS

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Calcium ions (Ca2+) influx to mitochondrial matrix is crucial for the life of a cell. Mitochondrial calcium uniporter (mtCU) is a protein complex which consists of the pore-forming subunit (MCU) and several regulatory subunits. MtCU is the main contributor to inward Ca2+ currents through the inner mitochondrial membrane. Extensive investigations of mtCU involvement into normal and pathological molecular pathways started from the moment of discovery of its molecular components. A crucial role of mtCU in the control of these pathways is now recognized in both health and disease. In particular, impairments of mtCU function have been demonstrated for cardiovascular and skeletal muscle-associated pathologies. This review summarizes the current state of knowledge on mtCU structure, regulation, and function in different types of muscle tissues in health and disease.

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Rescuing infusion of miRNA-1 prevents cardiac remodeling in a heart-selective miRNA deficient mouse

Cited by 13 publications

References 26 publications

A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy

A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy

LncRNA SUMO1P3 Aggravates Doxorubicin-Induced Cardiomyocyte Apoptosis by Targeting miR-93-5p / Bin1

Mitochondrial Calcium Uniporter Structure and Function in Different Types of Muscle Tissues in Health and Disease

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