MicroRNAs and cardiac pathology

Latronico, Michael V.G.; Condorelli, Gianluigi

doi:10.1038/nrcardio.2009.56

Cited by 285 publications

(206 citation statements)

References 119 publications

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“…Emerging studies show them to be important modulators of cardiovascular development (41) and angiogenesis (25), and aberrant miRNA expression is associated with cardiac arrhythmia, cardiac hypertrophy, and arterial stenosis (42). They are implicated in arterial hyperplasia through regulation of proliferation and phenotype switching of vascular smooth muscle cells (43).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-10a regulation of proinflammatory phenotype in athero-susceptible endothelium in vivo and in vitro

Fang¹,

Shi²,

Manduchi

et al. 2010

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

392

375

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A chronic proinflammatory state precedes pathological change in arterial endothelial cells located within regions of susceptibility to atherosclerosis. The potential contributions of regulatory microRNAs to this disequilibrium were investigated by artery site-specific profiling in normal adult swine. Expression of endothelial microRNA10a (miR-10a) was lower in the athero-susceptible regions of the inner aortic arch and aorto-renal branches than elsewhere. Expression of Homeobox A1 (HOXA1), a known miR-10a target, was up-regulated in the same locations. Endothelial transcriptome microarray analysis of miR-10a knockdown in cultured human aortic endothelial cells (HAEC) identified IκB/NF-κB-mediated inflammation as the top category of up-regulated biological processes. Phosphorylation of IκBα, a prerequisite for IκBα proteolysis and NF-κB activation, was significantly up-regulated in miR-10a knockdown HAEC and was accompanied by increased nuclear expression of NF-κB p65. The inflammatory biomarkers monocyte chemotactic protein 1 (MCP-1), IL-6, IL-8, vascular cell adhesion molecule 1 (VCAM-1), and E-selectin were elevated following miR-10a knockdown. Conversely, knockin of miR10a (a conservative 25-fold increase) inhibited the basal expression of VCAM-1 and E-selectin in HAEC. Two key regulators of IκBα degradation-mitogen-activated kinase kinase kinase 7 (MAP3K7; TAK1) and β-transducin repeat-containing gene (βTRC)-contain a highly conserved miR-10a binding site in the 3′ UTR. Both molecules were up-regulated by miR-10a knockdown and suppressed by miR-10a knockin, and evidence of direct miR-10a binding to the 3′ UTR was demonstrated by luciferase assay. Comparative expression studies of endothelium located in athero-susceptible aortic arch and athero-protected descending thoracic aorta identified significantly up-regulated MAP3K7, βTRC, phopho-IκBα, and nuclear p65 expression suggesting that the differential expression of miR-10a contributes to the regulation of proinflammatory endothelial phenotypes in athero-susceptible regions in vivo.β-transducing repeat-containing gene | hemodynamics | mitogen-activated kinase kinase kinase 7 | NF-κB

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Section: Discussionmentioning

confidence: 99%

MicroRNA-10a regulation of proinflammatory phenotype in athero-susceptible endothelium in vivo and in vitro

Fang¹,

Shi²,

Manduchi

et al. 2010

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

392

375

View full text Add to dashboard Cite

show abstract

“…Several studies have reported that some miRNAs are either increased (e.g., miR-195) [27] or decreased (e.g., miR-1, miR-133) [28] in response to dysregulated ion dynamics during pathological heart conditions. Importantly, alterations in the expression of miRNA may underlie the process producing the dysfunctional cardiac excitability and arrhythmic death [29]. Another intriguing finding of miR-NA regulation by the microenvironment comes from the recent reports showing that miRNAs participate in cellular responses to osmotic stress in mammalian cells.…”

Section: Mirnas and Alterations Of Their Expression In Response To MImentioning

confidence: 99%

Ion channels/transporters as epigenetic regulators? —a microRNA perspective

Jiang

Zhang

Chan

2012

Sci. China Life Sci.

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MicroRNA (miRNA) alterations in response to changes in an extracellular microenvironment have been observed and considered as one of the major mechanisms for epigenetic modifications of the cell. While enormous efforts have been made in the understanding of the role of miRNAs in regulating cellular responses to the microenvironment, the mechanistic insight into how extracellular signals can be transduced into miRNA alterations in cells is still lacking. Interestingly, recent studies have shown that ion channels/transporters, which are known to conduct or transport ions across the cell membrane, also exhibit changes in levels of expression and activities in response to changes of extracellular microenvironment. More importantly, alterations in expression and function of ion channels/transporters have been shown to result in changes in miRNAs that are known to change in response to alteration of the microenvironment. In this review, we aim to summarize the recent data demonstrating the ability of ion channels/transporters to transduce extracellular signals into miRNA changes and propose a potential link between cells and their microenvironment through ion channels/transporters. At the same time, we hope to provide new insights into epigenetic regulatory mechanisms underlying a number of physiological and pathological processes, including embryo development and cancer metastasis. ion channel, miRNAs, epigenetic, microenvironment

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“…miRNAs play essential roles in numerous cellular and developmental processes, including intracellular signaling pathways and organ morphogenesis (Stefani and Slack, 2008). Aberrant expression of miRNAs is closely associated with initiation and progression of pathophysiologic processes including diabetes, cancer, and cardiovascular disease (Thum et al, 2008;Croce, 2009;Latronico and Condorelli, 2009;Pandey et al, 2009). However, the role of miRNAs in lung fibrosis d 7 (Fig.…”

Section: Br Ief Definitive Repor Tmentioning

confidence: 99%