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Changes of the hepatic proteome in murine models for toxically induced fibrogenesis and sclerosing cholangitis
Author(s) -
Henkel Corinna,
Roderfeld Martin,
Weiskirchen Ralf,
Berres MarieLuise,
Hillebrandt Sonja,
Lammert Frank,
Meyer Helmut E.,
Stühler Kai,
Graf Jürgen,
Roeb Elke
Publication year - 2006
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200600580
Subject(s) - proteome , hydroxyproline , hepatic fibrosis , fibrosis , blot , biology , ccl4 , western blot , pathogenesis , microbiology and biotechnology , pathology , chemistry , biochemistry , immunology , medicine , carbon tetrachloride , gene , organic chemistry
We investigated the changes in the hepatic proteome in murine models for toxic‐induced fibrogenesis and sclerosing cholangitis. A comprehensive comparison of protein changes observed is made and the mechanistical basis of the expression changes is discussed. Hepatic fibrosis was induced by repetitive intraperitoneal CCl 4 treatment of BALB/c mice or developed spontaneously in BALB/c‐ATP‐binding cassette, subfamily B, member 4 (Abcb4) knock out mice. Fibrosis was verified by a morphometric score and assessment of hydroxyproline content of liver tissue, respectively. The innovative difference in‐gel electrophoresis (DIGE) technique was used to analyse protein expression levels of the mouse proteome. Results were confirmed by Western blotting and real‐time RT‐PCR. In CCl 4 ‐induced fibrosis 20 out of 40 and in BALB/c‐ Abcb4 − / − mice 8 out of 28 differentially expressed proteins were identified utilizing DIGE. Only two proteins, selenium‐binding protein (Sbp2) and carbonic anhydrase 3, have been unidirectionally expressed ( i.e. down‐regulated) in both models. Relevant differences in the pathogenesis of toxically induced liver fibrosis and sclerosing cholangitis exist. The only novel protein with regard to liver fibrosis depicting a unidirectional expression pattern in both animal models was Sbp2. An explicit protein function could not be clarified yet.

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