RGD Reference Report - Correlation between microRNA expression levels and clinical parameters associated with chronic hepatitis C viral infection in humans. - Rat Genome Database

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Correlation between microRNA expression levels and clinical parameters associated with chronic hepatitis C viral infection in humans.

Authors: Marquez, Rebecca T  Bandyopadhyay, Sarmistha  Wendlandt, Erik B  Keck, Kathy  Hoffer, Brandon A  Icardi, Michael S  Christensen, Randolph N  Schmidt, Warren N  McCaffrey, Anton P 
Citation: Marquez RT, etal., Lab Invest. 2010 Dec;90(12):1727-36. doi: 10.1038/labinvest.2010.126. Epub 2010 Jul 12.
RGD ID: 41404667
Pubmed: PMID:20625373   (View Abstract at PubMed)
DOI: DOI:10.1038/labinvest.2010.126   (Journal Full-text)

MicroRNAs (miRNAs) are small RNAs that regulate gene expression pathways. Previous studies have shown interactions between hepatitis C virus (HCV) and host miRNAs. We measured miR-122 and miR-21 levels in HCV-infected human liver biopsies relative to uninfected human livers and correlated these with clinical patient data. miR-122 is required for HCV replication in vitro, and miR-21 is involved in cellular proliferation and tumorigenesis. We found that miR-21 expression correlated with viral load, fibrosis and serum liver transaminase levels. miR-122 expression inversely correlated with fibrosis, liver transaminase levels and patient age. miR-21 was induced ∼twofold, and miR-122 was downregulated on infection of cultured cells with the HCV J6/JFH infectious clone, thus establishing a link to HCV. To further examine the relationship between fibrosis and the levels of miR-21 and miR-122, we measured their expression levels in a mouse carbon tetrachloride fibrosis model. As in the HCV-infected patient samples, fibrotic stage positively correlated with miR-21 and negatively correlated with miR-122 levels. Transforming growth factor β (TGF-β) is a critical mediator of fibrogenesis. We identified SMAD7 as a novel miR-21 target. SMAD7 is a negative regulator of TGF-β signaling, and its expression is induced by TGF-β. To confirm the relationship between miR-21 and the TGF-β signaling pathway, we measured the effect of miR-21 on a TGF-β-responsive reporter. We found that miR-21 enhanced TGF-β signaling, further supporting a relationship between miR-21 and fibrosis. We suggest a model in which miR-21 targeting of SMAD7 could increase TGF-β signaling, leading to increased fibrogenesis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MIR21Humanhepatitis C disease_progressionIEP  RGD 
Mir21Rathepatitis C disease_progressionISOMIR21 (Homo sapiens) RGD 
Mir21aMousehepatitis C disease_progressionISOMIR21 (Homo sapiens) RGD 
MIR21Humanliver cirrhosis disease_progressionISOMir21a (Mus musculus) RGD 
Mir21Ratliver cirrhosis disease_progressionISOMir21a (Mus musculus) RGD 
Mir21aMouseliver cirrhosis disease_progressionIEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir21  (microRNA 21)

Genes (Mus musculus)
Mir21a  (microRNA 21a)

Genes (Homo sapiens)
MIR21  (microRNA 21)


Additional Information