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Treatment of Human Airway Smooth Muscle Cells with a Geranylgeranyltransferase Inhibitor Blocks Agonist-Induced Actin Reorganization



Treatment of Human Airway Smooth Muscle Cells with a Geranylgeranyltransferase Inhibitor Blocks Agonist-Induced Actin Reorganization



Anesthesiology Abstracts of Scientific Papers Annual Meeting (2001): Abstract No A-1304



To determine whether RhoA isoprenylation (geranylgeranylation) is required for agonist-induced actin cytoskeleton reorganization (measured as an increase in the fluorescence intensity ratio of stained F- and G-actin), cultured human airway smooth muscle cells were treated for 72 hours with inhibitors of geranylgeranyltransferase-I. Geranylgeranyltransferase inhibitor (GGTI-2147 or GGTI-286) pretreatment completely blocked the increase in F- to G-actin fluorescence intensity ratio when cells were stimulated with lysophosphatidic acid (LPA), endothelin, or carbachol. In contrast, LPA or endothelin induced actin cytoskeleton reorganization in cells treated with a farnesyltransferase inhibitor (FTI-277) to inactivate Ras. Forskolin-induced adenylyl cyclase activity was inhibited by carbachol in GGTI-2147-pretreated cells, demonstrating that the effect of geranylgeranyltransferase-I inhibition on stress-fiber formation was not due to uncoupling of signaling between the heterotrimeric Gi (the Ggamma-subunit is isoprenylated) and distal effectors. These results demonstrate that selective geranylgeranyltransferase-I inhibitors can inhibit agonist-induced actin reorganization. .

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Accession: 035980501

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