Hepatic α-smooth muscle actin expression in hepatitis C patients before and after interferon therapy

M. A. Khan, J. E. Poulos, E. M. Brunt, L. Li, H. Solomon, R. S. Britton, B. R. Bacon, A. M. Di Bisceglie

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Background/Aims: The mechanism of hepatic fibrogenesis with chronic viral hepatitis is not well understood. Persistent activation of hepatic stellate cells is felt to play a role in the development of fibrogenesis and progression to cirrhosis. Methodology: We determined the expression of hepatic α-smooth muscle actin, a marker of hepatic stellate cell activation, in 29 patients with chronic hepatitis C and varying degrees of liver injury and fibrosis. In addition to a baseline evaluation, we assessed the effect of interferon therapy on α-smooth muscle actin expression in 11 patients, including 6 with a sustained response to therapy. Specimens were evaluated by light microscopy for grade of inflammation and stage of fibrosis. Expression of α-smooth muscle actin was assessed semiquantitatively by immunohistochemical staining. Results: At baseline, all patients had α-smooth muscle actin expressed within the liver without an obvious correlation with the severity of liver injury. However, among sustained responders, a reduction in hepatic necroinflammatory activity was associated with a trend towards a decrease in α-smooth muscle actin expression. This however did not reach statistical significance. Conclusions: Hepatic α-smooth muscle actin expression, as a marker of hepatic stellate cell activation appears reversible and tends to correlate with necroinflammatory activity.

Original languageEnglish
Pages (from-to)212-215
Number of pages4
Issue number37
StatePublished - 2001


  • Alpha smooth muscle actin
  • Fibrogenesis
  • Hepatitis C
  • Interferon
  • Stellate cell


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