NDLI: Systems analysis reveals down-regulation of a network of pro-survival miRNAs drives the apoptotic response in dilated cardiomyopathy.

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Year: 2014 Volume: 10

Systems analysis reveals down-regulation of a network of pro-survival miRNAs drives the apoptotic response in dilated cardiomyopathy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Isserlin, Ruth Merico, Daniele Wang, Dingyan Vuckovic, Dajana Bousette, Nicolas Gramolini, Anthony O. Bader, Gary D. Emili, Andrew
Description	Author Affiliation: Isserlin R ( The Donnelly Centre, University of Toronto, 160 College Street, Toronto, Ontario, Canada M5S 3E1. andrew.emili@utoronto.ca.)
Abstract	Apoptosis is a hallmark of multiple etiologies of heart failure, including dilated cardiomyopathy. Since microRNAs are master regulators of cardiac development and key effectors of intracellular signaling, they represent novel candidates for understanding the mechanisms driving the increased dysfunction and loss of cardiomyocytes during cardiovascular disease progression. To determine the role of cardiac miRNAs in the apoptotic response, we used microarray technology to monitor miRNA levels in a validated murine phospholambam mutant model of dilated cardiomyopathy. 24 miRNAs were found to be differentially expressed, most of which have not been previously linked to dilated cardiomyopathy. We showed that individual silencing of 7 out of 8 significantly down-regulated miRNAs (mir-1, -29c, -30c, -30d, -149, -486, -499) led to a strong apoptotic phenotype in cell culture, suggesting they repress pro-apoptotic factors. To identify putative miRNA targets most likely relevant to cell death, we computationally integrated transcriptomic, proteomic and functional annotation data. We showed the dependency of prioritized target abundance on miRNA expression using RNA interference and quantitative mass spectrometry. We concluded that down regulation of key pro-survival miRNAs causes up-regulation of apoptotic signaling effectors that contribute to cardiac cell loss, potentially leading to system decompensation and heart failure.
File Format	HTM / HTML
ISSN	1742206X
e-ISSN	17422051
DOI	10.1039/c4mb00265b
Journal	Molecular BioSystems
Issue Number	1
Volume Number	11
Language	English
Publisher	Royal Society of Chemistry
Publisher Date	2015-01-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology Discipline Biochemistry Apoptosis Genetics Cardiomyopathy, Dilated Gene Expression Regulation Gene Regulatory Networks Micrornas Animals Pathology Cell Survival Cluster Analysis Computational Biology Disease Models, Animal Down-regulation Gene Expression Profiling Mice Mice, Transgenic Rna, Messenger Reproducibility Of Results Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Biotechnology

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