Nonmuscle myosin light-chain kinase mediates neutrophil transmigration in sepsis-induced lung inflammation by activating beta2 integrins.

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 beta(2) integrins. Our results demonstrate that MYLK-mediated activation of beta(2) integrins through Pyk2 links beta(2) integrin signaling to the actin motile machinery of neutrophils.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Xu J,Gao XP,Ramchandran R,Zhao YY,Vogel SM,Malik AB

doi

10.1038/ni.1628

subject

Has Abstract

pub_date

2008-08-01 00:00:00

pages

880-6

issue

8

eissn

1529-2908

issn

1529-2916

pii

ni.1628

journal_volume

9

pub_type

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