Molecular Biology of the Cell Sign up for new MBC in Press e-TOCs!

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
QUICK SEARCH:   [advanced]


     

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
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
E04-01-0011v1
16/1/73    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cirri, P.
Right arrow Articles by Ramponi, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cirri, P.
Right arrow Articles by Ramponi, G.

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




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. Zhuang, Q. Pu, B. Ceacareanu, Y. Chang, M. Dixit, and A. Hassid
Chronic insulin treatment amplifies PDGF-induced motility in differentiated aortic smooth muscle cells by suppressing the expression and function of PTP1B
Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H163 - H173.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2004 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.