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Published ahead of print on January 23, 2004, doi:10.1165/rcmb.2003-0406OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 6, June 2004, 901-907

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Submitted on November 12, 2003
Revised on January 22, 2004

KGF stimulates alveolar type II cell proliferation through the ERK and PI3 Kinase pathways

Joshua Portnoy1*, Douglas Curran-Everett2, and Robert J Mason1

1 Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado, USA; Department of Medicine, Pulmonary Division, University of Colorado Health Sciences Center, Denver, Colorado, USA, 2 Department of Medicine, Division of Biostatistics, National Jewish Medical and Research Center, Denver, Colorado, USA; Department of Preventive Medicine and Biometrics and of Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, Colorado, USA

* To whom correspondence should be addressed. E-mail: portnoyj{at}njc.org.

Keratinocyte Growth Factor (KGF or FGF-7) stimulates alveolar type II cell proliferation, but little is known about the signaling pathways involved. We investigated the role of the ERK (p42/44 MAP kinase) and PI3 kinase pathways on alveolar type II cell proliferation and differentiation. Rat type II cells were cultured on tissue culture plastic and Matrigel in the presence or absence of KGF and specific chemical inhibitors PD98059, LY294002 and rapamycin at various concentrations. Proliferation was measured by thymidine incorporation and DNA quantitation, and differentiation was measured by expression of surfactant protein A and alkaline phosphatase. We demonstrate that KGF activates distal effectors of the PI3 kinase pathway, PKB/Akt and p70S6 kinase as well as p42/44 MAP kinase proteins. Inhibition of these pathways with PD98059, LY294002 or rapamycin inhibited type II cell proliferation but had no significant effect on differentiation. KGF did not activate the JNK or p38 MAP kinase pathways. We conclude that the p42/44 MAP kinase and PI3 kinase pathways are important in regulating alveolar type II cell proliferation in response to KGF.




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