Abstract
We investigated the role of cysteinyl leukotriene (CysLT) receptors on leukotriene D 4-induced actin reorganization and the signaling pathways of the response in human bronchial smooth muscle cells. The effects of leukotriene D 4 on actin reorganization in human bronchial smooth muscle cells were evaluated by dual-fluorescence labeling of filamentous (F) and monomeric (G) actin with fluorescein isothiocyanate (FITC)-labeled phalloidin and Texas Red-labeled DNase I, respectively. Leukotriene D 4 (100 nM) induced actin reorganization in the presence and absence of extracellular Ca 2+. The CysLT type 1 (CysLT 1) receptor antagonist ONO 1078 (4-oxo-8(−)[ p-(4-phenylbutyloxy) benzoylamino]-2-(tetrazol-5-yl)-4 H-1-benzopyran hemihydrate) inhibited leukotriene D 4-induced actin reorganization. Pretreatment with pertussis toxin, C3 exoenzyme, or tyrosine kinase inhibitors significantly reduced leukotriene D 4-induced actin reorganization. However, phosphatidylinositol-3-kinase and protein kinase C inhibitors had little effect on these responses. These results suggest that leukotriene D 4-induced actin reorganization in human bronchial smooth muscle cells is extremely dependent on the CysLT 1 receptor coupled with pertussis toxin-sensitive G protein, Rho GTPases and tyrosine phosphorylation pathways.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
