MicroRNA profiling during rat ventricular maturation: A role for miR‐29a in regulating cardiomyocyte cell cycle re‐entry

Cao, Xin; Wang, Jue; Wang, Zhenhua; Du, Juan; Yuan, Xin; Huang, Weicong; Meng, Jiao; Gu, Haiyong; Nie, Yu; Ji, Bingyang; Hu, Shengshou; Zheng, Zhe

doi:10.1016/j.febslet.2013.01.075

Cited by 61 publications

(49 citation statements)

References 26 publications

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“…Several of these abundant miRNAs were shown to inhibit cell cycle progression in cultured cardiomyocytes (41) and in vivo (42). A similar difference in mir-29a(4) expression between fetal and adult skeletal muscle indicates a more ubiquitous antiproliferative role of mir-29a(4).…”

Section: Discussionmentioning

confidence: 98%

Comparative RNA-sequencing analysis of myocardial and circulating small RNAs in human heart failure and their utility as biomarkers

Akat

Moore-McGriff

Morozov

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

215

210

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Heart failure (HF) is associated with high morbidity and mortality and its incidence is increasing worldwide. MicroRNAs (miRNAs) are potential markers and targets for diagnostic and therapeutic applications, respectively. We determined myocardial and circulating miRNA abundance and its changes in patients with stable and end-stage HF before and at different time points after mechanical unloading by a left ventricular assist device (LVAD) by small RNA sequencing. miRNA changes in failing heart tissues partially resembled that of fetal myocardium. Consistent with prototypical miRNAtarget-mRNA interactions, target mRNA levels were negatively correlated with changes in abundance for highly expressed miRNAs in HF and fetal hearts. The circulating small RNA profile was dominated by miRNAs, and fragments of tRNAs and small cytoplasmic RNAs. Heart-and muscle-specific circulating miRNAs (myomirs) increased up to 140-fold in advanced HF, which coincided with a similar increase in cardiac troponin I (cTnI) protein, the established marker for heart injury. These extracellular changes nearly completely reversed 3 mo following initiation of LVAD support. In stable HF, circulating miRNAs showed less than fivefold differences compared with normal, and myomir and cTnI levels were only captured near the detection limit. These findings provide the underpinning for miRNA-based therapies and emphasize the usefulness of circulating miRNAs as biomarkers for heart injury performing similar to established diagnostic protein biomarkers.exRNA | body fluids | miRNA-mRNA regulation | development | cardiovascular disease

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Section: Discussionmentioning

confidence: 98%

Comparative RNA-sequencing analysis of myocardial and circulating small RNAs in human heart failure and their utility as biomarkers

Akat

Moore-McGriff

Morozov

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

215

210

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“…The miRNA-RBP cooperation and competition add an additional level of gene expression regulation. This type of interplay can also be involved in transcription regulation during cardiac development as well as in heart failure due to the extensive changes in miRNA (Cao et al 2013 ) and RBP expression levels ; and our unpublished data) in both processes.…”

Section: Mirnas/rbp Interplaymentioning

confidence: 64%

“…Additionally, Dicer is up-regulated in human patients with DCM and heart failure (Chen et al 2008b ) and large miRNA expression alteration is present in cardiac disease (van Rooij et al 2006 ;Sayed et al 2007 ). miRNAs target numerous mRNAs such as cell cycle and extracellular matrix genes being responsible for their regulation during heart development and in cardiac pathologies (van Rooij et al 2008 ;Ikeda and Pu 2010 ;Porrello et al 2011b ;Cao et al 2013 ). However, miRNAs can also bind mRNA-encoding RBPs, regulating RBP expression (Fig.…”

Section: Mirnas/rbp Interplaymentioning

confidence: 99%

RNA-Binding Proteins in Heart Development

Giudice

Cooper

2014

Systems Biology of RNA Binding Proteins

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RNA-binding proteins (RBPs) are key players of posttranscriptional regulation occurring during normal tissue development. All tissues examined thus far have revealed the importance of RBPs in the regulation of complex networks involved in organ morphogenesis, maturation, and function. They are responsible for controlling tissue-specific gene expression by regulating alternative splicing, mRNA stability, translation, and poly-adenylation. The heart is the first organ form during embryonic development and is also the first to acquire functionality. Numerous remodeling processes take place during late cardiac development since fetal heart first adapts to birth and then undergoes a transition to adult functionality. This physiological remodeling involves transcriptional and posttranscriptional networks that are regulated by RBPs. Disruption of the normal regulatory networks has been shown to cause cardiomyopathy in humans and animal models. Here we review the complexity of late heart development and the current information regarding how RBPs control aspects of postnatal heart development. We also review how activities of RBPs are modulated adding complexity to the regulation of developmental networks.

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“…53,54 CCND2 can be regulated by miR-26a, miR-154, miR-206 and miR-29a. 50,[55][56][57] Herein, CCND2 was negatively regulated by miR-26b-5p in GC-2 cells at 2 mT and 3 mT. However, there was no obvious change in CCND2 or miR-26b-5p expression between the exposure and sham groups at 1 mT.…”

Section: Discussionmentioning

confidence: 86%

Overexpression of miR-26b-5p regulates the cell cycle by targeting CCND2 in GC-2 cells under exposure to extremely low frequency electromagnetic fields

Liu

et al. 2016

Cell Cycle

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The increasing prevalence of extremely low frequency electromagnetic fields (ELF-EMFs) exposure has raised considerable public concern regarding the potential hazardous effects of ELF-EMFs on male reproductive function. Increasing evidence indicates that miRNAs are necessary for spermatogenesis and male fertility. However, the regulation of miRNA expression and the roles of miRNAs in response to ELFEMFs remain unclear. In our study, mouse spermatocyte-derived GC-2 cells were intermittently exposed to a 50 Hz ELF-EMF for 72 h (5 min on/10 min off) at magnetic field intensities of 1 mT, 2 mT and 3 mT. MiR26b-5p was differentially expressed in response to different magnetic field intensities of ELF-EMFs. The host gene CTDSP1 showed an unmethylation status in GC-2 cells at different magnetic field intensities of ELF-EMF exposure. MiR-26b-5p had no significant, obvious influence on the cell viability, apoptosis or cell cycle of GC-2 cells. However, the overexpression of miR-26b-5p significantly decreased the percentage of G0/G1 phase cells and slightly increased the percentage of S phase cells compared to the sham group that was exposed to a 50 Hz ELF-EMF. Computational algorithms identified Cyclin D2 (CCND2) as a direct target of miR-26b-5p. MiR-26b-5p and a 50 Hz ELF-EMF altered the expression of CCND2 at both the mRNA and protein levels. Overexpressed miR-26b-5p in GC-2 cells can change the mRNA expression of CCND2 following 50 Hz ELF-EMF at 3 mT. These findings demonstrate that miR-26b-5p could serve as a potential biomarker following 50 Hz ELF-EMF exposure, and miR-26b-5p-CCND2-mediated cell cycle regulation might play a pivotal role in the biological effects of ELF-EMFs.

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MicroRNA profiling during rat ventricular maturation: A role for miR‐29a in regulating cardiomyocyte cell cycle re‐entry

Cited by 61 publications

References 26 publications

Comparative RNA-sequencing analysis of myocardial and circulating small RNAs in human heart failure and their utility as biomarkers

Comparative RNA-sequencing analysis of myocardial and circulating small RNAs in human heart failure and their utility as biomarkers

RNA-Binding Proteins in Heart Development

Overexpression of miR-26b-5p regulates the cell cycle by targeting CCND2 in GC-2 cells under exposure to extremely low frequency electromagnetic fields

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