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Submitted on November 12, 2003
Accepted on March 29, 2004
Department of Medicine, Göttingen; Institute of Pathology, Otto-von-Guericke-Universität, Magdeburg; Children's Hospital-Biochemistry, Universitätsklinikum Eppendorf, Hamburg, Germany; Dipartimento di Biologia Sperimentale, Ambientale e Applicata, Università di Genova, Genova, Italy
* To whom correspondence should be addressed. E-mail: braulke{at}uke.uni-hamburg.de.
Hepatic stellate cells (HSC) play a pivotal role in hepatic tissue repair and fibrogenesis. IGF-I has been considered as mitogenic signal for activation and proliferation of HSC in vitro. In the present study IGF-I and IGFBP gene expression was studied in a model of acute liver injury induced by a single intragastric dose of carbon tetrachloride (CCl4) in adult rats. Northern blot analysis revealed a marked increase of IGFBP-1 mRNA levels with a maximum between 3 and 9 h after CCl4 application whereas steady-state mRNA levels of IGF-I were only moderately altered. In situ hybridization experiments demonstrated that this increase of IGFBP-1 mRNA was due to a strong expression of IGFBP-1 in the perivenous region 6 to 12 h after CCl4 application extending to the midzonal region of the acinus within 24 to 48 h. Consequently, a prominent immunostaining for IGFBP-1 was observed in perivenous areas with a maximum at 24 to 48 h after intoxication. Preincubation of "early cultured" HSC with a non-phosphorylated IGFBP-1 from human amniotic fluid resulted in a 3.4-fold increase of IGF-I induced DNA synthesis. The mitogenic effect of IGF-I was also potentiated when HSC were co-cultivated with IGFBP-1 overexpressing BHK-21 cells as compared with non-transfected cells. These data suggest that IGFBP-1 released during early steps of liver tissue damage and repair may interact with HSC and potentiate the sensitivity to mitogenic signals of IGF-I.
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