MicroRNAs in the Myocyte Enhancer Factor 2 (MEF2)-regulated Gtl2-Dio3 Noncoding RNA Locus Promote Cardiomyocyte Proliferation by Targeting the Transcriptional Coactivator Cited2

Clark, Amanda; Naya, Francisco J.

doi:10.1074/jbc.m115.672659

Cited by 59 publications

(54 citation statements)

References 56 publications

(53 reference statements)

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“…For example, the expression of muscle-related genes is regulated coordinately by well-known transcriptional factors including serum response factor (SRF), myocyte enhancer factor 2 (MEF2) and other transcription factors (13).…”

Section: Biology Of Mir-499 In Cardiomyocyte Developmentmentioning

confidence: 99%

Circulating miR-499 as a potential biomarker for acute myocardial infarction

Xin¹,

Yang²,

Han³

2016

Ann. Transl. Med.

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Acute myocardial infarction (AMI), a common heart disease that may lead to chronic heart failure, is the leading cause of morbidity and mortality worldwide. MicroRNAs (miRNAs) are small non-coding RNAs that mediate the expression of target genes. Recently, a number of miRNAs are emerging as potential biomarkers of AMI. MiRNA-499 is a newly discovered member of miRNAs, and is mainly expressed in myocardium, the circulating levels of miRNA-499 was increased in AMI patients. This review summarizes the latest advances in the miRNA-499 study and discusses the potential of miRNA-499 to be a biomarker of AMI. Acute myocardial infarction (AMI) is one of the leading causes of morbidity and mortality worldwide, thus an effective and accurate diagnostic biomarker would be needed to help decrease the mortality of AMI patients. One of the traditional biomarkers for AMI is troponin. Circulating troponin levels rise around 3 hours after the onset of chest pain, due to the relative delayed release time of troponin. It is widely believed that a rapid and correct diagnosis of AMI has an important impact on patients' treatment and prognosis. Therefore, earlier biomarkers than troponin with both high sensitivity and specificity remain to be needed. MicroRNAs (miRNAs) are endogenous small non-coding RNAs of less than 22 nucleotides that are implicated in nearly all cellular events including cell differentiation and proliferation as well as the pathogenesis of certain human diseases (1,2). Recently, a number of findings support the notion of the implication of miRNAs in the development and progression of cardiovascular diseases (3). The plasma levels of miRNA-1, -133a, -133b, and -499-5p are upregulated in AMI patient, and represent novel biomarkers of cardiac damage. Several reviews have provided an over-view of biology of miRNA-1, miRNA-133b, -499-5p and their involvement in cardiovascular physiology and pathology, and discussed the potential of these miRNAs to become a novel biomarker of AMI and even an effective therapeutics agent (4-8). miRNA-499 is a newly discovered member of miRNAs encoded by myosin gene family, and its expression level in plasma was elevated in the patients with AMI, a common heart disease that is the leading cause of morbidity and mortality worldwide (9). A previous study compared the diagnostic performance of miRNA-499 and some traditional biomarkers like SMB, cTnI, cTnT, CK-MB, CK, LDH, and concluded that miRNA-499 was present in plasma earlier than other conventional biomarkers of AMI, pointing to the likelihood that miR-499 can be a vital molecule in the early diagnosis of AMI. This study also found that the circulating level of miR-499 correlated well with circulating troponin I

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Section: Biology Of Mir-499 In Cardiomyocyte Developmentmentioning

confidence: 99%

Circulating miR-499 as a potential biomarker for acute myocardial infarction

Xin¹,

Yang²,

Han³

2016

Ann. Transl. Med.

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“…However, the role of miRNAs in the adaptation of the RV to pressure and volume overload and the transition to RV failure remains unclear. We focused on miR-495 in right heart hypertrophy for the following reasons: (1) miR-495 was initially identified as one of the deregulated miRNAs in the Gtl2-Dio3 locus; (2) miR-495 is upregulated in multiple models of cardiac disease and is associated with prohypertrophy; its inhibition in stressed cardiomyocytes thus attenuates the pathological growth response [17]; and (3) the Gtl2-Dio3 locus is also regulated by myocyte enhancer factor 2 (MEF2) in cardiac muscle [15,17]. MEF2 has been implicated in RV development, regulating the metabolic, contractile, and angiogenic genes [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies found that Mef2a knockout mice displayed increased mortality in the first week of life, with severe, spontaneous RV chamber dilation [16]. miR-495 was able to induce the proliferation of neonatal cardiomyocytes in vitro [15]. It was also upregulated as prohypertrophic molecules in multiple models of cardiac diseases [17].…”

Section: Introductionmentioning

confidence: 94%

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Attenuation of MicroRNA-495 Derepressed PTEN to Effectively Protect Rat Cardiomyocytes from Hypertrophy

Chen

2018

Cardiology

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Background: The effect of microRNA (miR)-495 on cardiomyocyte hypertrophy was explored by investigating the expression of proteins in the phosphatidylinositol 3-kinase (PI3K)/Akt signal pathway. Methods: The study used a rat model of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) administration (60 mg/kg) for 2 weeks. Arterial wall thickness and right ventricular hypertrophy were examined by hematoxylin and eosin (HE) staining in the lungs and hearts. The expression level of miR-495 and PTEN was analyzed by quantitative (q)PCR and Western blotting. From the cellular level, we used loss-of-function approaches to investigate the functional roles of miR-495 in cardiac hypertrophy induced by angiotensin II (Ang II) with immunoﬂuorescence, qPCR, and Western blotting. Results: The results showed that upregulation of miR-495 markedly influenced the expression of hypertrophic markers, including the induction of nppa and the inhibition of myh6. In contrast, a reduction in the level of miR-495 attenuated an Ang II-induced hypertrophic reaction. Furthermore, PTEN was identified as a potential target of miR-495 by a bioinformatics algorithm. Luciferase analysis and Western blot analysis confirmed that the contribution of miR-495 to cardiomyocyte hypertrophy may partly be through targeting PTEN. Conclusions: Attenuation of miR-495 derepressed PTEN to effectively protect rat cardiomyocytes from hypertrophy.

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“…Wang observed that miR-495 could regulate Bmi-1 to arrest the G1 to S phase transition in breast cancer [8]. Very recently, miR-495 was found to participate in Wnt signaling pathway regulation in cardiomyocyte proliferation [9], whose main function is to promote cell proliferation and differentiation [10,11]. However, little else is known about the reverse chain of miR-495, miR-495-3p, the implications of its function and expression in colon cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-495-3p facilitates colon cancer cell proliferation via Wnt/β-catenin signaling pathway by restraining Wnt inhibitory factor

Lin¹,

Tong²,

Li³

et al. 2017

Trop. J. Pharm Res

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Purpose: To demonstrate whether miR-495-3p promote the occurrence of colon cancer and development of colon cancer stem cells by inhibiting Wnt inhibitory factor (WIF1). Methods: The level of MiRNA and mRNA in cells were tested by real-time polymerase chain reaction (RT-PCR). Cell viability was assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell spheroid formation was measured by colony assay. Expression protein was

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MicroRNAs in the Myocyte Enhancer Factor 2 (MEF2)-regulated Gtl2-Dio3 Noncoding RNA Locus Promote Cardiomyocyte Proliferation by Targeting the Transcriptional Coactivator Cited2

Cited by 59 publications

References 56 publications

Circulating miR-499 as a potential biomarker for acute myocardial infarction

Circulating miR-499 as a potential biomarker for acute myocardial infarction

Attenuation of MicroRNA-495 Derepressed PTEN to Effectively Protect Rat Cardiomyocytes from Hypertrophy

MiR-495-3p facilitates colon cancer cell proliferation via Wnt/β-catenin signaling pathway by restraining Wnt inhibitory factor

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