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Nonmuscle myosin light chain kinase activity modulates radiation-induced lung injury.

Abstract：

:Radiotherapy as a primary treatment for thoracic malignancies induces deleterious effects, such as acute or subacute radiation-induced lung injury (RILI). Although the molecular etiology of RILI is controversial and likely multifactorial, a potentially important cellular target is the lung endothelial cytoskeleton that regulates paracellular gap formation and the influx of macromolecules and fluid to the alveolar space. Here we investigate the central role of a key endothelial cytoskeletal regulatory protein, the nonmuscle isoform of myosin light chain kinase (nmMLCK), in an established murine RILI model. Our results indicate that thoracic irradiation significantly augmented nmMLCK protein expression and enzymatic activity in murine lungs. Furthermore, genetically engineered mice harboring a deletion of the nmMLCK gene (nmMLCK(-/-) mice) exhibited protection from RILI, as assessed by attenuated vascular leakage and leukocyte infiltration. In addition, irradiated wild-type mice treated with two distinct MLCK enzymatic inhibitors, ML-7 and PIK (peptide inhibitor of kinase), also demonstrated attenuated RILI. Taken together, these data suggests a key role for nmMLCK in vascular barrier regulation in RILI and warrants further examination of RILI strategies that target nmMLCK.

journal_name

Pulm Circ

journal_title

Pulmonary circulation

authors

Wang T,Mathew B,Wu X,Shimizu Y,Rizzo AN,Dudek SM,Weichselbaum RR,Jacobson JR,Hecker L,Garcia JG

doi

10.1086/686491

subject

Has Abstract

pub_date

2016-06-01 00:00:00

pages

234-9

issue

2

eissn

2045-8932

issn

2045-8940

pii

PC2013283

journal_volume

6

pub_type

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