Article abstract
Nature Immunology 9, 880 - 886 (2008)
Published online: 29 June 2008 | doi:10.1038/ni.1628
Nonmuscle myosin light-chain kinase mediates neutrophil transmigration in sepsis-induced lung inflammation by activating 
2 integrins
Jingsong Xu1,2,3, Xiao-Pei Gao1,3, Ramaswamy Ramchandran1, You-Yang Zhao1, Stephen M Vogel1 & Asrar B Malik1
Abstract
Nonmuscle myosin light-chain kinase (MYLK) mediates increased lung vascular endothelial permeability in lipopolysaccharide-induced lung inflammatory injury, the chief cause of the acute respiratory distress syndrome. In a lung injury model, we demonstrate here that MYLK was also essential for neutrophil transmigration, but that this function was mostly independent of myosin II regulatory light chain, the only known substrate of MYLK. Instead, MYLK in neutrophils was required for the recruitment and activation of the tyrosine kinase Pyk2, which mediated full activation of 
2 integrins. Our results demonstrate that MYLK-mediated activation of 2 integrins through Pyk2 links 2 integrin signaling to the actin motile machinery of neutrophils.
- Department of Pharmacology, University of Illinois College of Medicine, Chicago, Illinois 60612, USA.
- Department of Dermatology, and Center for Lung and Vascular Biology, University of Illinois College of Medicine, Chicago, Illinois 60612, USA.
- These authors contributed equally to this work.
Correspondence to: Jingsong Xu1,2,3 e-mail: jingsong@uic.edu
Correspondence to: Asrar B Malik1 e-mail: abmalik@uic.edu
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