2. Aim and objectives. The inhibition of HSC activation by HDAC complex inhibition could offer possibilities for therapeutic intervention during liver fibrogenesis and fibroproliferative disease on the whole. The underlying molecular mechanism of this HDAC inhibitor-dependent stellate cell inhibition is largely unknown primarily because the HDAC inhibitor used in the initial studies on stellate cells were large spectrum and there are 11 HDACs identified so far(11,12). Moreover, most research on HDAC-repressor complexes is carried out in immortalized cell lines. As a result, the presence or activity of the known HDAC-repressor complexes has not been demonstrated in many primary cells like hepatic stellate cells. Characterization of HDAC-complexes and understanding their mechanism of action during stellate cell activation would be an important step towards the development of a more efficient anti-fibrotic therapy. Taken together, there is a need for an analysis of HDAC complexes that function during fibrogenesis. The aim of this project is to isolate and characterize these complexes in vitro and in vivo
Effective start/end date1/01/0931/12/12

    Flemish discipline codes

  • Electrical and electronic engineering
  • Basic sciences
  • Biological sciences

    Research areas

  • Fibrosis, Hepatic Stellate Cells, Histon (de)acetylation, Stellate cell activation, Liver Cell Transplantation, Portal hypertension, Sinusoidal Cells, Liver Sinusoidal Cells, Cell Biology, Cytoskeleton, Fat-Storing Cells, NASH / NAFLD, Intermediate Filaments, liver stem / progenitor cells, Flow Cytometry, Metabolic Syndrome, Chirrosis

ID: 3293572