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Research ArticleArticle

Selective Down-Regulation of c-jun Gene Expression by Pentoxifylline and c-jun Antisense Interrupts Platelet-Derived Growth Factor Signaling: Pentoxifylline Inhibits Phosphorylation of c-Jun on Serine 73

Theresa C. Peterson, Marc R. Peterson, Harold A. Robertson, Matthew During and Michael Dragunow
Molecular Pharmacology June 2002, 61 (6) 1476-1488; DOI: https://doi.org/10.1124/mol.61.6.1476
Theresa C. Peterson
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Marc R. Peterson
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Harold A. Robertson
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Matthew During
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Michael Dragunow
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Abstract

Platelet-derived growth factor (PDGF) signals through several pathways, including mitogen-activated protein (MAP) kinase, Jun kinase, and C kinase, and stimulates proliferation of fibroblasts. Pentoxifylline inhibits PDGF-driven proliferation of fibroblasts. We have reported that pentoxifylline did not inhibit binding of PDGF to its specific cell-surface receptors or PDGF receptor phosphorylation. In this study, we investigated the effect of PDGF on the expression of c-fos and c-jun, because c-fos and c-jun form activator protein-1 complexes that stimulate genes involved in proliferation. We determined whether pentoxifylline would alter the expression of c-fos and c-jun. Our results indicate that PDGF induced the expression of both c-fos and c-jun. Pentoxifylline effectively reduced c-jun gene expression, which had been up-regulated by PDGF, but did not alter c-fos gene expression. The lack of effect on c-fos supports other studies from this laboratory, which indicate that pentoxifylline did not inhibit PDGF activation of MAP kinase. Treatment of fibroblasts with a phosphothioate c-jun antisense oligodeoxynucleotide reduced the levels of c-Jun protein and blocked PDGF-stimulated proliferation, suggesting a critical role for c-jun in PDGF-mediated proliferation. Combination of pentoxifylline and c-jun antisense suggested that they were likely inhibiting PDGF-stimulated proliferation at a single site in the PDGF signaling pathway. These results suggest that pentoxifylline inhibits PDGF-stimulated proliferation by selectively decreasing c-jun expression. To further define the mechanism of action of pentoxifylline, we assessed the effect of pentoxifylline on c-Jun and phosphorylated c-Jun immunoreactivity in cells treated with PDGF and cells that were transfected with wild-type c-jun plasmid using immunocytochemistry and Western blot analyses, and our results indicate that pentoxifylline inhibited phosphorylation of c-Jun on serine 73.

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Molecular Pharmacology: 61 (6)
Molecular Pharmacology
Vol. 61, Issue 6
1 Jun 2002
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Research ArticleArticle

Selective Down-Regulation of c-jun Gene Expression by Pentoxifylline and c-jun Antisense Interrupts Platelet-Derived Growth Factor Signaling: Pentoxifylline Inhibits Phosphorylation of c-Jun on Serine 73

Theresa C. Peterson, Marc R. Peterson, Harold A. Robertson, Matthew During and Michael Dragunow
Molecular Pharmacology June 1, 2002, 61 (6) 1476-1488; DOI: https://doi.org/10.1124/mol.61.6.1476

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Research ArticleArticle

Selective Down-Regulation of c-jun Gene Expression by Pentoxifylline and c-jun Antisense Interrupts Platelet-Derived Growth Factor Signaling: Pentoxifylline Inhibits Phosphorylation of c-Jun on Serine 73

Theresa C. Peterson, Marc R. Peterson, Harold A. Robertson, Matthew During and Michael Dragunow
Molecular Pharmacology June 1, 2002, 61 (6) 1476-1488; DOI: https://doi.org/10.1124/mol.61.6.1476
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