Abstract
We studied the mechanism of sphingosylphosphorylcholine (SPC)-induced contraction in feline ileal smooth muscle cells. Western blotting revealed that G protein subtypes of Gα i1, Gα i3 and Gα o existed in feline ileum. Gα i3 antibody penetration into permeabilized cells decreased SPC-induced contraction. In addition, incubation of [ 35S]guanosine 5′- O-(3-thiotriphosphate) ([ 35S]GTPγS) with membrane fraction increased its binding to Gα i3 subtype after SPC treatment, suggesting that the signalling pathways invoked by SPC were mediated by Gα i3 protein. MAPK kinase (MEK) inhibitor PD98059 blocked the contraction significantly, but p38 mitogen-activated protein kinase (MAPK) inhibitor SB202190 did not. Chelerythrine and neomycin also inhibited the contraction. However, cotreatment of PD98059 and chelerythrine showed no significant difference. Phosphorylation of p44/42 MAPK was increased by SPC treatment, which was reversed by pretreatment of inhibitors of signalling molecules that decreased SPC-induced contraction previously. The same result was obtained in the assay of MAPK activity.
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