Biochemical and biophysical research communications · 2001
Simultaneous induction of galectin-3 phosphorylated on tyrosine residue, p21(WAF1/Cip1/Sdi1), and the proliferating cell nuclear antigen at a distinctive period of repair of hepatocytes injured by CCl4.
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Yamazaki K, Kawai A, Kawaguchi M, Hibino Y, Li F, Sasahara M, Tsukada K, Hiraga K
Аннотация
The period of repair of hepatocytes injured by CCl4 and signaling proteins intrinsic to this period were examined. A 30 kDa polypeptide detected by immunoblot analysis using anti-phosphotyrosine antibody in livers from rats 48 to 72 h after administration of a single dose of CCl4 was identified as galectin-3 induced in cytoplasm of periportal hepatocytes and phosphorylated on tyrosine residue(s). Simultaneously, these hepatocytes induced p21(WAF1/Cip1/Sdi1) in the nucleus and the proliferating cell nuclear antigen in both the nucleus and the cytoplasm, suggesting that hepatocytes during this distinctive period are quiescent and repair cellular damage. Trabecular architecture of hepatocytes with the proliferating cell nuclear antigen only in the nucleus was found at 96 h. These findings indicate that galectin-3 is a novel member of signaling proteins downstream of tyrosine kinase, and suggest that it plays roles in supporting repair or survival of the injured hepatocytes rather than their proliferation that is likely to be initiated later than 72 h.
Предметные рубрики MeSH
AnimalsAntigens, DifferentiationBlotting, NorthernCarbon TetrachlorideCloning, MolecularCyclin-Dependent Kinase Inhibitor p21CyclinsCytoplasmFibrosisGalectin 3HepatocytesImmunoblottingImmunohistochemistryLiverPhosphorylationPhosphotyrosineProliferating Cell Nuclear AntigenRatsRats, WistarSignal TransductionTime FactorsTyrosine