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Am. J. Respir. Cell Mol. Biol., Volume 26, Number 1, January, 2002 99-104

The Role of the Receptor Tyrosine Kinase Ron in Nickel-Induced Acute Lung Injury

Susan A. McDowell, Ali Mallakin, Cindy J. Bachurski, Kenya Toney-Earley, Daniel R. Prows, Theresa Bruno, Klaus H. Kaestner, David P. Witte, Hector Melin-Aldana, Sandra J. F. Degen, George D. Leikauf, and Susan E. Waltz

Departments of Environmental Health, Molecular and Cellular Physiology, and Pulmonary and Critical Care Medicine, University of Cincinnati, Cincinnati; Divisions of Developmental Biology, Pulmonary Biology, Pathology, and Gastroenterology, Children's Hospital Research Foundation, Cincinnati, Ohio; and Department of Genetics, University of Pennsylvania Medical School, Philadelphia, Pennsylvania

Acute lung injury (ALI), a severe respiratory syndrome, develops in response to numerous insults and responds poorly to therapeutic intervention. Recently, cDNA microarray analyses were performed that indicated several pathogenic responses during nickel-induced ALI, including marked macrophage activation. Macrophage activation is mediated, in part, via the receptor tyrosine kinase Ron. To address the role of Ron in ALI, the response of mice deficient in the cytoplasmic domain of Ron (Ron tk-/-) were assessed in response to nickel exposure. Ron tk-/- mice succumb to nickel-induced ALI earlier, express larger, early increases in interleukin-6, monocyte chemoattractant protein-1, and macrophage inflammatory protein-2, display greater serum nitrite levels, and exhibit earlier onset of pulmonary pathology and augmented pulmonary tyrosine nitrosylation. Increases in cytokine expression and cellular nitration can lead to tissue damage and are consistent with the differences between genotypes in the early onset of pathology and mortality in Ron tk-/- mice. These analyses indicate a role for the tyrosine kinase receptor Ron in ALI.

Abbreviations: acute lung injury, ALI; granulocyte macrophage-colony stimulating factor, GM-CSF; hepatocyte growth factor-like protein/macrophage stimulating protein, HGFL/MSP; interferon-gamma , IFN-gamma ; interleukin, IL; inducible NO synthase, iNOS; monocyte chemotactic protein, MCP; macrophage migration inhibitory factor, MIF; macrophage inflammatory protein, MIP; nitric oxide, NO; phosphatidylinositol-3, PI-3; regulated upon activation, normal T cells expressed and secreted, RANTES; transforming growth factor, TGF; tumor necrosis factor, TNF.




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