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Originally published In Press as doi:10.1074/jbc.M110005200 on November 27, 2001

J. Biol. Chem., Vol. 277, Issue 7, 5236-5246, February 15, 2002
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Activation of SHIP by NADPH Oxidase-stimulated Lyn Leads to Enhanced Apoptosis in Neutrophils*

Shyra GardaiDagger , Ben B. Whitlock§, Cheryl Helgason, Dan Ambruso||, Valerie Fadok§, Donna Bratton§, and Peter M. Henson§**

From the Dagger  Departments of Pathology, University of Colorado Health Sciences Center, Denver, Colorado 80262, § Program in Cell Biology, Department of Pediatrics and Immunology, National Jewish Medical and Research Center, Denver, Colorado 80206, the  Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia V5Z 1L3, Canada, and the || Departments of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262

Neutrophils undergo rapid spontaneous apoptosis. Multiple antiapoptotic stimuli can inhibit this process via activation of the Akt pathway. However, despite no such effect singly, combined anti- and proapoptotic stimuli inhibit Akt activity, leaving the cells susceptible to accelerated apoptosis. The blockade of Akt activation depended on reduced phosphoinositide 3,4,5-trisphosphate levels but not decreased phosphatidylinositol 3-kinase activity, thus implicating the involvement of an inositol phosphatase. Evidence for SHIP involvement was provided by SHIP localization to membrane receptors and subsequent activation along with the observed inability of SHIP -/- neutrophils to exhibit enhanced apoptosis with the stimulus combination. Activation of SHIP was found to depend on Lyn activation, and this, in turn, required NADPH oxidase. Neutrophils from chronic granulomatous disease patients and Lyn -/- mice no longer responded to the combined stimuli. Thus, we propose a role for oxidants and Lyn in SHIP regulation and suggest a novel mechanism for regulating neutrophil apoptosis.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

** To whom all correspondence should be addressed: National Jewish Medical and Research Center, D508, 1400 Jackson St., Denver, CO 80206. Tel.: 303-398-1380; Fax: 303-398-1381; E-mail: hensonp@NJC.org.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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