Significance of pSmad2/3 and Smad4 in hepatitis C virus-related liver fibrosis and hepatocellular carcinoma

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Moussa M.M.; Helal N.S.; Youssef M.M.

Journal: APMIS

Publisher: Blackwell Munksgaard

Publication Date: 20 June 2018

Volume / Issue: Volume 126 / Issue 6

Pages: 477–485

ISSN: 9034641

DOI: 10.1111/apm.12844

Scopus: View on Scopus

PubMed: 29924446

Document Type: Article

Authors and Affiliations

Moussa M.M., Pathology Department, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt; Helal N.S., Pathology Department, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt; Youssef M.M., Pharmacology and Toxicology Department, Egyptian-Russian University, Cairo, Egypt, Graduate School, Okinawa Institute of Science and Technology Graduate University, Okinawa, Japan

Abstract

Chronic hepatitis C (CHC) is a major public health problem, especially in Egypt. Risk of hepatocellular carcinoma (HCC) development increases as hepatitis C virus (HCV)-related liver diseases progress. Smads act as substrates for the transforming growth factor-beta (TGF-β) family of receptors. This study aims to assess hepatic expression of pSmad2/3 and Smad4 in CHC with different stages of fibrosis and grades of necro-inflammation as well as in HCC on top of CHC. This study was done on 33 core liver biopsies from patients with CHC (15 with early fibrosis and 18 with late fibrosis), 15 liver specimens from HCC cases on top of CHC, as well as five normal controls. pSmad2/3 and Smad4 show more immunopositivity, higher percentage of positive hepatocytes and stronger staining intensity in CHC with late fibrosis compared to early fibrosis. pSmad2/3 shows increase of the previous parameters in CHC with high grade activity than those with low activity. Smad4 shows increase of the previous parameters in HCC compared to CHC cases. pSmad2/3 and Smad4 can be used as diagnostic and/or prognostic markers for progression of HCV-related fibrosis to cirrhosis and further progression to HCC. © 2018 APMIS. Published by John Wiley & Sons Ltd

Keywords

HCV; Hepatocarcinogenesis; liver fibrosis; pSmad2/3; Smad4; Adult; Antibodies, Viral; Antigens, Viral; Carcinoma, Hepatocellular; Case-Control Studies; Disease Progression; Female; Gene Expression Regulation; Hepacivirus; Hepatitis C; Humans; Immunohistochemistry; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Smad2 Protein; Smad3 Protein; Smad4 Protein; Young Adult; alanine aminotransferase; albumin; alkaline phosphatase; aspartate aminotransferase; serum albumin; SMAD2 protein, human; SMAD3 protein, human; SMAD4 protein, human; virus antibody; virus antigen; alanine aminotransferase blood level; Article; aspartate aminotransferase blood level; controlled study; human; human cell; human tissue; immunoreactivity; liver cell; liver cell carcinoma; priority journal; protein expression; blood; case control study; disease exacerbation; genetics; isolation and purification; liver tumor; metabolism; virology

Citation Information

Scopus Citations: 9

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