NF-kB mediated miR-26a regulation in cardiac fibrosis. (Articolo in rivista)

Type
Label
  • NF-kB mediated miR-26a regulation in cardiac fibrosis. (Articolo in rivista) (literal)
Anno
  • 2013-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1002/jcp.24296 (literal)
Alternative label
  • Wei C(1), Kim IK1(1), Kumar S(1), Jayasinghe S(1), Hong N(1), Castoldi G(2), Catalucci D(3), Jones WK(4), Gupta S(1) (2013)
    NF-kB mediated miR-26a regulation in cardiac fibrosis.
    in Journal of cellular physiology (Online)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Wei C(1), Kim IK1(1), Kumar S(1), Jayasinghe S(1), Hong N(1), Castoldi G(2), Catalucci D(3), Jones WK(4), Gupta S(1) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://onlinelibrary.wiley.com/doi/10.1002/jcp.24296/abstract (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • (1)Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center, Scott & White, Central Texas Veterans Health Care System, Temple, Texas (2)Dipartimento di Medicina Clinica e Prevenzione, Universita'degli Studi di Milano-Bicocca, Monza, Italy (3)Biomedical and Genetic Research Institute, National Research Council, Milan, Italy (4)Department of Pharmacology and Cell Biophysics, University of Cincinnati, Cincinnati, Ohio (literal)
Titolo
  • NF-kB mediated miR-26a regulation in cardiac fibrosis. (literal)
Abstract
  • Micro-RNAs (miRNAs) are a class of small non-coding RNAs, recently emerged as a post-transcriptional regulator having a key role in various cardiac pathologies. Among them, cardiac fibrosis that occurs as a result from an imbalance of extracellular matrix proteins turnover and is a highly debilitating process that eventually lead to organ dysfunction. An emerging theme on is that miRNAs participate in feedback loop with transcription factors that regulate their transcription. NF-?B, a key transcription factor regulator controls a series of gene program in various cardiac diseases through positive and negative feedback mechanism. But, NF-?B mediated miRNA regulation in cardiac fibrosis remains obscure. Bioinformatics analysis revealed that miR-26a has targets collagen I and CTGF and possesses putative NF-?B binding element in its promoter region. Here, we show that inhibition of NF-?B in cardiac fibroblast restores miR-26a expression, attenuating collagen I, and CTGF gene expression in the presence of Ang II, conferring a feedback regulatory mechanism in cardiac fibrosis. The target genes for miR-26a were confirmed using 3?-UTR luciferase reporter assays for collagen I and CTGF genes. Using NF-?B reporter assays, we determine that miR-26a overexpression inhibits NF-?B activity. Finally, we show that miR-26a expression is restored along with the attenuation of collagen I and CTGF genes in cardiac specific IkBa triple mutant transgenic mice (preventing NF-?B activation) subjected to 4 weeks transverse aortic banding (TAC), compared to wild type (WT) mice. The data indicate a potential role of miR-26a in cardiac fibrosis and, offer novel therapeutic intervention (literal)
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