Δημοσίευση

TGF-β signaling is activated in patients with chronic HBV infection and repressed by SMAD7 overexpression after successful antiviral treatment.

ΤίτλοςTGF-β signaling is activated in patients with chronic HBV infection and repressed by SMAD7 overexpression after successful antiviral treatment.
Publication TypeJournal Article
Year of Publication2016
AuthorsArgentou, N., Germanidis G., Hytiroglou P., Apostolou E., Vassiliadis T., Patsiaoura K., Sideras P., Germenis A. E., & Speletas M.
JournalInflamm Res
Volume65
Issue5
Pagination355-65
Date Published2016 May
ISSN1420-908X
Λέξεις κλειδιάAdult, Aged, Antiviral Agents, Chronic Disease, Female, Fibrosis, Hepatitis B, Hepatitis C, Humans, Liver, Male, Middle Aged, Non-alcoholic Fatty Liver Disease, RNA, Messenger, Signal Transduction, Smad7 Protein, Transforming Growth Factor beta, Young Adult
Abstract

OBJECTIVES: Although animal studies demonstrated that Smad7 induction ameliorates TGF-β/SMAD-mediated fibrogenesis, its role in human hepatic diseases is rather obscure. Our study explored the activation status of TGF-β/activin pathway in patients with chronic liver diseases, and how it is affected by successful antiviral treatment in chronic HBV hepatitis (CHB).METHODS: Thirty-seven CHB patients (19 with active disease, 14 completely remitted on long-term antiviral treatment and 4 with relapse after treatment withdrawal), 18 patients with chronic HCV hepatitis, 12 with non-alcoholic fatty liver disease (NAFLD), and 3 controls were enrolled in the study. Liver mRNA levels of CTGF, all TGF-β/activin isoforms, their receptors and intracellular mediators (SMADs) were evaluated using qRT-PCR and were correlated with the grade of liver inflammation and fibrosis staging. The expression and localization of pSMAD2 and pSMAD3 were assessed by immunohistochemistry.RESULTS: TGF-β signalling is activated in CHB patients with active disease, while SMAD7 is up-regulated during the resolution of inflammation after successful treatment. SMAD7 overexpression was also observed in NAFLD patients exhibiting no or minimal fibrosis, despite the activation of TGF-β/activin signaling.CONCLUSIONS: SMAD7 overexpression might represent a mechanism limiting TGF-β-mediated fibrogenesis in human hepatic diseases; therefore, SMAD7 induction likely represents a candidate for novel therapeutic approaches.

DOI10.1007/s00011-016-0921-6
Alternate JournalInflamm. Res.
PubMed ID26856334

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