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Table of Contents
30, No. 4, 2012
Issue release date: September 2012
Section title: Original Paper
Cell Physiol Biochem 2012;30:905-914

Role of Kinase Suppressor of Ras-1 in Lipopolysaccharide-Induced Acute Lung Injury

Li X.a · Gulbins E.b · Zhang Y.a
aDepartment of Pharmacology & Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, VA; bInstitute of Molecular Biology, University of Duisburg-Essen, Essen
email Corresponding Author

Yang Zhang, Ph.D

Department of Pharmacology & Toxicology

Medical College of Virginia Campus, Virginia Commonwealth University, MMRB,

3rd Floor, Room 3048, 1220 East Broad Street, Richmond, VA 23298-0613 (USA)

Tel. +1804-828-0738, Fax +1804-828-4794, E-Mail yzhang3@vcu.edu

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Kinase suppressor of ras-1 (Ksr1) has been recently shown to be a central signaling molecule in the host response to Pseudomonas aeruginosa infections in the lung. Ksr1 functions to regulate the release of nitric oxide (NO)-radicals upon P. aeruginosa infections. Ksr1 also enhances Raf-1/MEK/ERK signaling and is involved in a variety of cellular responses, including cell differentiation, proliferation, and apoptosis. Here, we investigated whether Ksr1 is involved in the host immune response to lipopolysaccharide (LPS), one of the major components of gram-negative bacteria, in the lung. To this end, we induced an acute lung injury in wild type and Ksr1-deficient mice by intratracheal instillation of LPS. We found that LPS-induces acute lung injury, as characterized by cytokine expression, neutrophil infiltration and protein extrusion in wildtype mice. Ksr1-deficient mice showed a very similar reaction to LPS as the wildtype mice. In freshly isolated alveolar macrophages from wild type and Ksr1-deficient mice, LPS increased ERK activation, nuclear translocation of NFĸB and expression of inflammatory cytokines and chemokines in a similar pattern. Inhibition of Src or Raf-1 blocked LPS-induced ERK activation. Taken together, these findings indicate that Ksr1 plays a dispensable role in LPS-induced ERK activation in alveolar macrophages and does not contribute to the development of acute lung injury in the LPS model.

© 2012 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: August 06, 2012
Published online: August 28, 2012
Issue release date: September 2012

Number of Print Pages: 10
Number of Figures: 2
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

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