Changes in Regulatory MicroRNA Expression in Myocardium of Heart Failure Patients on Left Ventricular Assist Device Support

Schipper, Marguérite E.I.; Kuik, J. van; Jonge, N. De; Dullens, H. F. J.; Weger, Roel A. de

doi:10.1016/j.healun.2008.09.005

Cited by 47 publications

(36 citation statements)

References 23 publications

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“…A limited qPCR study of four miRs also found that LVAD treatment normalized abnormal expression, but suggested that this effect was more pronounced in ischaemic cardiomyopathy. 79 The remarkable sensitivity of the miR signature to biomechanical support, which is known to favourably effect both cardiac performance and remodelling, parallels regulated expression of Dicer, the critical enzyme for processing to mature miRs (see above). Dicer levels are decreased in human heart failure, but normalized by LVAD treatment.…”

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confidence: 99%

microRNAs in heart disease: putative novel therapeutic targets?

Condorelli

Latronico

Dorn

2010

European Heart Journal

150

115

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microRNAs (miRs) are short, approximately 22-nucleotide-long non-coding RNAs involved in the control of gene expression. They guide ribonucleoprotein complexes that effect translational repression or messenger RNA degradation to targeted messenger RNAs. miRs were initially thought to be peculiar to the developmental regulation of the nematode worm, in which they were first described in 1993. Since then, hundreds of different miRs have been reported in diverse organisms, and many have been implicated in the regulation of physiological processes of adult animals. Of importance, misexpression of miRs has been uncovered as a pathogenic mechanism in several diseases. Here, we first outline the biogenesis and mechanism of action of miRs, and then discuss their relevance to heart biology, pathology, and medicine.--

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confidence: 99%

microRNAs in heart disease: putative novel therapeutic targets?

Condorelli

Latronico

Dorn

2010

European Heart Journal

150

115

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“…[7][8][9][10] Furthermore, unique miRNA expression profiles had been detected in human cardiomyopathy and pressure overloaded cardiac hypertrophy, and many miRNAs were dysregulated in the heart, indicating the involvement of miRNAs in cardiac diseases. 7,[11][12][13][14][15][16][17] It is well established that Ang II-mediated cardiac remodeling is a multigene disorder that involves a global change in the gene expression profile. miRNA analysis provides a novel mechanism for this alteration.…”

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confidence: 99%

MicroRNA Let-7i Negatively Regulates Cardiac Inflammation and Fibrosis

Wang

et al. 2015

Hypertension

104

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Abstract-Angiotensin II stimulates fibroblast proliferation and substantially alters gene expression patterns leading to cardiac remodeling, but the mechanisms for such differences are unknown. MicroRNAs are a novel mechanism for gene expression regulation. Herein, we tested the miRNA and mRNA expression patterns in mouse heart using microarray assay and investigated their role in angiotensin II-induced cardiac remodeling. We found that let-7i was dynamically downregulated in angiotensin II-infused heart at day 3 and 7 and had the most targets that were mainly associated with cardiac inflammation and fibrosis. Overexpression or knockdown of let-7i in cultured cardiac fibroblasts demonstrated that let-7i played an inhibitory effect on the expression of its targets interleukin-6 and collagens. Furthermore, delivery of let-7i to mouse significantly inhibited angiotensin II-induced cardiac inflammation and fibrosis in a dose-dependent manner. Conversely, knockdown of let-7i aggravated this effect. Together, our results clearly demonstrate that let-7i acts as a novel negative regulator of angiotensin II-induced cardiac inflammation and fibrosis by suppressing the expression of interleukin-6 and multiple collagens in the heart and may represent a new potential therapeutic target for treating hypertensive cardiac fibrosis. (Hypertension. 2015;66:776-785.

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“…Morphological changes during LVAD support were paralleled by changes in collagen turnover and expression of genes encoding for structural collagens (Type I and III;Bruggink et al, 2006b;2007). So, the minor changes observed in expression of ECM genes in the present study may imply that most ECM changes are induced post-transcriptionally, either by micro-RNA regulation (Schipper et al, 2008) or in the matrix itself (e.g. by MMP).…”

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confidence: 52%