ABSTRACT
<p><b>OBJECTIVE</b>To study the role of insulin-like growth factor II receptor in free silica-induced transdifferentiation of primary rat lung fibroblasts.</p><p><b>METHODS</b>Rat lung fibroblasts and rat alveolar macrophages were cultured. A transdifferentiation model of primary rat lung fibroblasts was induced by free silica. Levels of α-SMA protein, IGF-IIR protein and mRNA were measured by immunocytochemistry, Western blot and RT-PCR, respectively. Lung fibroblasts were treated with Wortmannin.</p><p><b>RESULTS</b>The expression levels of α-SMA and IGF-IIR increased with the increasing free silica concentration and decreased after Wortmannin was used.</p><p><b>CONCLUSION</b>The IGF-IIR plays an important role in free silica-induced transdifferentiation of primary rat lung fibroblasts.</p>
Subject(s)
Animals , Male , Rats , Base Sequence , Cell Differentiation , Physiology , Cells, Cultured , DNA Primers , Fibroblasts , Lung , Cell Biology , RNA, Messenger , Genetics , Rats, Sprague-Dawley , Receptor, IGF Type 2 , Genetics , Physiology , Silicon Dioxide , PharmacologyABSTRACT
The expression of cancer gene products of insuline-like growth factor Ⅱ (IGF-Ⅱ),IGF-Ⅱ receptors (IGF-Ⅱ-R),and colony-stimulating factor 1 receptors (CSF-1-R) /c-fms in 17 cases of human primary hepatic cancer,the non-cancerous liver tissue adjacent to the cancer,and normal liver tissue was studied with immunocytochemistry (ABC),Western blot and Northern blot techniques.It was found that the expression of IGF-Ⅱ,IGF-Ⅱ-R and CSF-1-R was significantly higher in the cancers than in normal liver tissues,and the expression of IGF-Ⅱ and IGF-Ⅱ-R was higher in the non-cancerous liver tissues than in the cancers.It was noteworthy that the expression of IGF-Ⅱ in both the cancerous and non-cancerous hepatic tissues was characterized by its fetal type.However the expression of CSF-1-R was distinctly higher in the cancers than in the non-cancerous hepatic tissue.These findings,the authors believe,imply that the aberrant overexpression of IGF-Ⅱ,IGF-Ⅱ-R and CSF-l-R might be related to the mechanism of auto-crine-stimulated growtth of the cells of human primary hepatic cancer.