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Am. J. Respir. Cell Mol. Biol., Volume 26, Number 2, February, 2002 224-230

Monocyte Survival Factors Induce Akt Activation and Suppress Caspase-3

Anuj Goyal, Yijie Wang, Mandy M. Graham, Andrea I. Doseff, Nitin Y. Bhatt, and Clay B. Marsh

Division of Pulmonary and Critical Care Medicine and the Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University College of Medicine and Public Health, Columbus, Ohio

A number of inflammatory cytokines and growth factors promote monocyte survival; however, the biochemical events stimulated by these factors are poorly defined. We previously showed that the monocyte survival factor macrophage colony-stimulating factor (M-CSF) activated monocyte survival through a PI 3-kinase-dependent pathway resulting in the phosphorylation of Akt and the suppression of the activation of caspase-3. Because other cytokines and bacterial cell wall products also induce monocyte survival, we hypothesized that these factors may also suppress caspase-3 and caspase-9 activation and activate Akt in human monocytes. To test this hypothesis, we found that interleukin (IL)-1beta , tumor necrosis factor (TNF)-alpha , lipopolysaccharide (LPS), granulocyte macrophage-colony-stimulating factor (GM-CSF), and IL-18 appeared to suppress DNA fragmentation, caspase-9, and caspase-3 activation in human monocytes. Moreover, these stimuli appeared to induce the serine and threonine phosphorylation of Akt, which was reduced by the PI 3-kinase inhibitor LY294002. Using in vitro kinase assays, M-CSF appeared to induce more Akt activity than did the other survival factors. Treatment of monocytes with either LY294002 or wortmannin resulted in caspase-3 activation in the presence of these survival factors. These results suggest that monocyte survival factors may suppress DNA fragmentation, caspase-9, and caspase-3 activation in a PI 3-kinase-dependent manner, perhaps through the activation of Akt.

Abbreviations: interleukin, IL; lactate dehydrogenase, LDH; lipopolysaccharide, LPS; tumor necrosis factor-alpha , TNF-alpha .




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