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MBC in Press, published online ahead of print November 3, 2004
Mol. Biol. Cell 10.1091/mbc.E04-01-0011

A more recent version of this article appeared on January 1, 2005
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Submitted on January 8, 2004
Revised on October 12, 2004
Accepted on October 26, 2004

Insulin Inhibits PDGF-induced Cell Proliferation

P. Cirri, M. L. Taddei, P. Chiarugi, F. Buricchi, A. Caselli, P. Paoli, E. Giannoni, G. Camici, G. Manao, G. Raugei, and G. Ramponi*

Dipartimento di Scienze Biochimiche, Università di Firenze, 50134 Firenze, Italy

Monitoring Editor: Carl-Henrik Heldin

Cellular behavior can be considered to be the result of a very complex spatial and temporal integration of intracellular and extracellular signals. These signals arise from serum soluble factors as well as from cell-substrate or cell-cell interactions. The current approach in mitogenesis studies is generally to analyze the effect of a single growth factor on serum starved cells. In this context, a metabolic hormone like insulin is found to be a mitogenic agent in many cellular types. In the present study we have considered the effect of insulin stimulation in PDGF -activated NIH-3T3 and C2C12 cells. Our results show that insulin is able to inhibit strongly both NIH-3T3 and C2C12 cell growth induced by PDGF, one of the most powerful mitotic agents for these cell types. This inhibitory effect of insulin is due primarily to a premature down-regulation of the PDGF receptor. Thus, when NIH-3T3 or C2C12 cells are stimulated with both PDGF and insulin we observe a decrease in PDGF receptor phosphorylation with respect to cells treated with PDGF alone. In particular, we find that costimulation with insulin leads to a reduced production of H2O2 with respect to cell stimulation with PDGF alone. The relative low concentration of H2O2 in PDGF/insulin costimulated cell leads to a limited down-regulation of PTPs and, consequently, to a reduced PDGF receptor phosphorylation efficiency. The latter is very likely to be responsible for the insulin-dependent inhibition of PDGF-R mitogenic signaling.

*Corresponding author. E-mail: ramponi{at}scibio.unifi.it




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[Abstract] [Full Text] [PDF]


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