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Papers In Press, published online ahead of print September 6, 2002
Department of Pulmonary Medicine, Baylor College of Medicine, Houston, TX 77030
Corresponding Author: boriek{at}bcm.tmc.edu
In the diaphragm muscle we tested the hypothesis that MAP kinase signaling pathways are activated by mechanical stress and such signaling pathway is dependent on the direction in which mechanical stress is applied. Although equal magnitudes of mechanical stress were applied axially and transversely a greater level of activation of ERK1/2, p38, Raf-1, p90RSK, Elk-1 and the DNA-binding activity of AP-1 transcription factor was produced when the muscle was stretched transversely than when stretched axially. A significant up-regulation in protein tyrosine phosphorylation was observed in axially or transversely loaded diaphragm muscles and the activation of ERK1/2 was completely inhibited by genistein (protein tyrosine kinase inhibitor). Pretreatment of muscles with wortmannin (phosphoinositide 3-kinase inhibitor), TMB-8 (antagonist of intracellular calcium release), GF109203X (PKC inhibitor), PD98059 (MEK1/2 inhibitor) blocked the activation of ERK1/2 kinases in response to axial but not to transverse loading. On the other hand, pretreatment of muscles with PKA inhibitors H-7 and KT5720 completely suppressed the activation of ERK1/2 in response to transverse loading only. Taken together with the alterations of MAP kinases and the findings of elevations of downstream transcription targets, our data are consistent with two distinct MAP kinase signal transduction pathways in response to mechanical stress.
J. Biol. Chem, 10.1074/jbc.M203654200
Submitted on April 16, 2002
Revised on September 4, 2002
Accepted on September 5, 2002
Distinct signaling pathways are activated in response to mechanical stress applied axially and transversely to skeletal muscle fibers
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