Relations between circulating microRNAs (miR-21, miR-26, miR-29, miR-30 and miR-133a), extracellular matrix fibrosis and serum markers of fibrosis in dilated cardiomyopathy

Rubiś, Paweł; Totoń‐Żurańska, Justyna; Wiśniowska‐Śmiałek, Sylwia; Holcman, Katarzyna; Kołton-Wróż, Maria; Wołkow, Paweł; Wypasek, Ewa; Natorska, Joanna; Rudnicka-Sosin, Lucyna; Pawlak, Agnieszka; Kozanecki, Artur; Podolec, Piotr

doi:10.1016/j.ijcard.2016.11.279

Cited by 39 publications

(36 citation statements)

References 26 publications

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“…Two microlitres of extracted RNA was used to perform reverse transcription with a TaqMan Advanced MicroRNA cDNA Synthesis Kit (Life Technologies). qPCR was conducted on 384‐well plates with TaqMan Advanced Master Mix and TaqMan Advanced Assays targeting: hsa‐miR‐21‐5p, hsa‐miR‐29b‐3p, hsa‐miR‐30c‐5p, hsa‐miR‐133a‐3p, hsa‐mir‐26a‐5p and hsa‐miR‐423‐3p . Fifteen microlitre reactions were prepared with pipetting station Bravo (Agilent Technologies), and a real‐time reaction was run and read on CFX384 Real‐Time PCR Detection System (Bio‐Rad).…”

Section: Methodsmentioning

confidence: 99%

The relationship between myocardial fibrosis and myocardial microRNAs in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events

Rubiś

Totoń‐Żurańska

Wiśniowska‐Śmiałek

et al. 2018

J Cellular Molecular Medi

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It is unknown whether fibrosis‐associated microRNAs: miR‐21, miR‐26, miR‐29, miR‐30 and miR‐133a are linked to cardiovascular (CV) outcome. The study evaluated the levels of extracellular matrix (ECM) fibrosis and the prevalence of particular microRNAs in patients with dilated cardiomyopathy (DCM) to investigate any correlation with CV events. Methods: Seventy DCM patients (48 ± 12 years, EF 24.4 ± 7.4%) underwent right ventricular biopsy. The control group was comprised of 7 patients with CAD who underwent CABG and intraoperative biopsy. MicroRNAs were measured in blood and myocardial tissue via qPCR. The end‐point was a combination of CV death and urgent HF hospitalization at the end of 12 months. There were differential levels of circulating and myocardial miR‐26 and miR‐29 as well as myocardial miR‐133a when the DCM and CABG groups were compared. Corresponding circulating and myocardial microRNAs did not correlate with one another. There was no correlation between microRNA and ECM fibrosis. By the end of the 12‐month period of the study, CV death had occurred in 6 patients, and a further 19 patients required urgent HF hospitalization. None of the circulating microRNAs was a predictor of the combined end‐point; however, myocardial miR‐133a was an independent predictor in unadjusted models (HR 1.53; 95% CI 1.14‐2.05; P < .004) and adjusted models (HR 1.57; 95% CI 1.14‐2.17; P < .005). The best cut‐off value for the miR‐133a level for the prediction of the combined end‐point was 0.74 ΔCq, with an AUC of 0.67. The absence of a correlation between the corresponding circulating and myocardial microRNAs calls into question their cellular source. This study sheds new light on the role of microRNAs in ECM fibrosis in DCM, which warrants further exploration.

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Section: Methodsmentioning

confidence: 99%

The relationship between myocardial fibrosis and myocardial microRNAs in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events

Rubiś

Totoń‐Żurańska

Wiśniowska‐Śmiałek

et al. 2018

J Cellular Molecular Medi

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“…A, Venn diagram generated by http://bioinformatics.psb.ugent.be/webtools/Venn/). Combined with previous studies, 15 candidate upstream miRNAs which are related to ECM were chosen for further assays: miR‐17 [Yu et al, ], miR‐449a [Han et al, ], miR‐33a [Li et al, ], miR‐15b [Kang et al, ], miR‐29c [Chuang et al, ], miR‐25 [Divakaran et al, ], miR‐155 [Sipert et al, ], miR‐24 [Wang et al, ], miR‐29b [Wang et al, ], miR‐29a [James et al, ], miR‐23b [Zhao et al, ], miR‐34a [Lichner et al, ], miR‐17 [Liu et al, ], miR‐204 [Chen et al, ], and miR‐21 [Rubis et al, ] (Fig. A).…”

Section: Resultsmentioning

confidence: 99%

The Role of c‐SKI in Regulation of TGFβ‐Induced Human Cardiac Fibroblast Proliferation and ECM Protein Expression

Wang

Guo

Shen

et al. 2017

J of Cellular Biochemistry

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Cardiac fibrosis is characterized by over-deposition of extracellular matrix (ECM) proteins and over-proliferation of cardiac fibroblast, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. Transforming growth factor β 1 (TGFβ1) is as an essential inducing factor of cardiac fibrosis. C-Ski protein has been identified as an inhibitory regulator of TGFβ signaling. In the present study, we revealed the repressive effect of c-Ski on TGFβ1-induced human cardiac fibroblast (HCFB) proliferation and ECM protein increase (Collagen I and α-SMA). Moreover, miR-155 and miR-17 could inhibit SKI mRNA expression by direct binding to the 3'UTR of SKI, so as to reduce c-Ski protein level. Either miR-155 inhibition or miR-17 inhibition could reverse TGFβ1-induced HCFB proliferation and ECM protein increase. Taken together, we provided a potential therapy to treat cardiac fibrosis by inhibiting miR-155/miR-17 so as to restore the repressive effect of c-Ski on TGFβ1 signaling. J. Cell. Biochem. 118: 1911-1920, 2017. © 2017 Wiley Periodicals, Inc.

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“…Moreover, multiple studies have demonstrated that miR-133a-3p can be involved in regulating a variety of cardiovascular diseases, including cardiomyopathy [30], cardiac remodeling [31], heart failure (HF) [32], and myocardial ischemic injury [33]. However, elevation of miR-133a-3p reduces hypoxia-induced, oxidative stress-induced and ERS-induced cardiomyocyte apoptosis in vitro [22].…”

Section: Discussionmentioning

confidence: 99%

MiR-133a-3p transferred by circulating microvesicles derived from myocardial ischemic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury

Zhao

Zhu

Shang

et al. 2020

Preprint

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Background Microvesicles (MVs) are submicron membrane vesicles as mediators of intercellular communication. The aim of our study was to investigate protective mechanism of circulating MVs derived from ischemic preconditioning (IPC-MVs) on myocardial I/R injury. Results Administration of IPC-MVs reduced infarct size and activity of lactate dehydrogenase (LDH) in myocardial I/R injury in vivo. Meanwhile, IPC-MVs could increase cell viability and reduce LDH activity in hypoxia/reoxygenation (H/R) injured H9c2 cells in vitro. Microarray analysis demonstrated that miR-133a-3p expression in IPC-MVs increased apparently compared with Sham-MVs. We found that miR-133a-3p increased cell viability, decreased LDH activity and apoptosis , as well as suppressed H/R-induced endoplasmic reticulum stress (ERS). MVs induced by hypoxic preconditioning enriched with FAM-miR-133a-3p allowed the transfer of miR-133a-3p to target cells. In addition, miR-133a-3p was significantly increased in H/R injured H9c2 cells by treatment with IPC-MVs. Epidermal growth factor receptor (EGFR) is a target gene of miR-133a-3p. AG1478 (EGFR inhibitor) significantly increased cell viability, decreased LDH activity and ERS-induced apoptosis in H9c2 cells under H/R injury. Conclusions The findings of this study showed that IPC-MVs exerted cardioprotective effects by transferring miR-133a-3p into H/R injured cardiomyocytes targeting EGFR, thus attenuating ERS-induced apoptosis. MiR-133a-3p transferred by IPC-MVs may provide a novel therapy for myocardial I/R injury.

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Relations between circulating microRNAs (miR-21, miR-26, miR-29, miR-30 and miR-133a), extracellular matrix fibrosis and serum markers of fibrosis in dilated cardiomyopathy

Cited by 39 publications

References 26 publications

The relationship between myocardial fibrosis and myocardial microRNAs in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events

The relationship between myocardial fibrosis and myocardial microRNAs in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events

The Role of c‐SKI in Regulation of TGFβ‐Induced Human Cardiac Fibroblast Proliferation and ECM Protein Expression

MiR-133a-3p transferred by circulating microvesicles derived from myocardial ischemic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury

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