Histone Deacetylases in Hepatic Stellate Cells

Inge Mannaerts, Nele Nuytten, Albert Geerts, Leonardus Van Grunsven

Research output: Chapter in Book/Report/Conference proceedingMeeting abstract (Book)


Transdifferentiation of hepatic stellate cells (HSC) to myofibroblastic cells (MF) is a central event in liver fibrogenesis. Understanding molecular mechanisms that underlie this cellular event provides pivotal insights into development of new therapeutic modalities for cirrhosis. Stellate cell activation by liver injury leads to a phenotypic transdifferentiation characterized by loss of vitamin A and extensive production of extracellular matrix. This process can be mimicked in vitro by culturing freshly isolated hepatic stellate cells. The use of the histone deacetylase inhibitor (HDAC-I) trichostatin A in these cultures has shown that histone deacetylases (HDACs) might play a role in the pathogenesis of liver fibrosis. Here we show that the class I specific HDAC-I, Valproic acid, can influence the transdifferentiation from quiescent to activated HSCs in culture. Immunohistochemistry shows class I HDACs expression in cells of healthy and fibrotic livers. During in vitro and in vivo cell activation the HDAC class I protein expression alters. Further studies will enable us to identify possible HDAC complexes and their possible functions during in vitro and in vivo stellate cell activation.
Original languageEnglish
Title of host publicationProceedings 2008 BSCDB Spring meeting
Number of pages1
Publication statusPublished - 2008
EventFinds and Results from the Swedish Cyprus Expedition: A Gender Perspective at the Medelhavsmuseet - Stockholm, Sweden
Duration: 21 Sep 200925 Sep 2009


ConferenceFinds and Results from the Swedish Cyprus Expedition: A Gender Perspective at the Medelhavsmuseet


  • liver fibrosis
  • stellate cells
  • histone deacetylases


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