Selective inhibition of the platelet-derived growth factor signal transduction pathway by a protein-tyrosine kinase inhibitor of the -phenylaminopyrimidine class .

Buchdunger E ; Zimmermann J ; Mett H ; Meyer T ; Muller M ; Regenass U ; Lydon NB

CIBA Pharmaceuticals Division , Oncology Research Department , CIBA-Geigy Limited , Basel , Switzerland .

Proc Natl Acad Sci U S A 92 : 2558-62 ( 1995)

Abstract
The platelet-derived growth factor ( PDGF ) receptor is a member of the transmembrane growth factor receptor protein family with intrinsic protein-tyrosine kinase activity . We describe a potent protein-tyrosine kinase inhibitor ( CGP 53716 ) that shows selectivity for the PDGF receptor in vitro and in the cell . The compound shows selectivity for inhibition of PDGF-mediated events such as PDGF receptor autophosphorylation , cellular tyrosine phosphorylation , and c-fos mRNA induction in response to PDGF stimulation of intact cells . In contrast , ligand-induced autophosphorylation of the epidermal growth factor ( EGF ) receptor , insulin receptor , and the insulin-like growth factor I receptor , as well as c-fos mRNA expression induced by EGF , fibroblast growth factor , and phorbol ester , was insensitive to inhibition by CGP . In antiproliferative assays , the compound was approximately -fold more potent in inhibiting PDGF-mediated growth of v-sis-transformed BALB/c 3T3 cells relative to inhibition of EGF-dependent BALB/Mk cells , interleukin-3-dependent FDC-P1 cells , and the T24 bladder carcinoma line . When tested in vivo using highly tumorigenic v-sis- and human c-sis-transformed BALB/c 3T3 cells , CGP showed antitumor activity at well-tolerated doses . In contrast , CGP 53716 did not show antitumor activity against xenografts of the A431 tumor , which overexpresses the EGF receptor . These findings suggest that CGP 53716 may have therapeutic potential for the treatment of diseases involving abnormal cellular proliferation induced by PDGF receptor activation .

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Platelet-derived growth factor receptor expression after neural grafting in a rat model of Parkinson 's disease .

Ballagi AE ; Odin P ; Othberg-Cederstrom A ; Smits A ; Duan WM ; Lindvall O ; Funa K

Ludwig Institute for Cancer Research , Biomedical Center , Uppsala , Sweden .

Cell Transplant 3 : 453-60 ( 1994)

Abstract
Platelet-derived growth factor ( PDGF ) has trophic effect on dopaminergic neurons in vitro . We have previously shown dynamic changes in the expression of PDGF in embryonic mesencephalic grafts and surrounding host striatal tissue following intracerebral transplantation in a rat model of Parkinson 's disease . In this study the expression of the PDGF receptors was examined in the same model using immunohistochemistry . Most ventral mesencephalic ( VM ) cells from E13-E15 rat embryos possessed both PDGF alpha- and beta-receptors before implantation . Double immunofluorescence staining revealed that about 10% of the cells also expressed tyrosine hydroxylase ( TH ) . The PDGF alpha-receptor was detectable in the graft up to 1 wk after transplantation but had disappeared at 3 wk . In the host tissue , scattered glial cells were positive for the alpha-receptor but the expression was unchanged following transplantation . The beta-receptor expression almost completely disappeared from the grafted tissue by 4 h following transplantation , and only a few cells of the host striatum showed immunoreactivity . However , after 3 wk beta-receptor positive cells were again detectable in the graft . These cells appeared to be endothelial cells as identified by an antibody against von Willebrand 's factor . Our data suggest that PDGF might act locally on embryonic dopaminergic cells in an autocrine or juxtacrine manner before and shortly after transplantation , and on surrounding glial cells in a paracrine manner after transplantation . Furthermore , PDGF-BB might influence neovascularization in the graft .