Tunicamycin inhibits prostaglandin F2α receptor-mediated phosphoinositide hydrolysis in cultured rat astrocytes
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Effect of tunicamycin, an inhibitor of N-linked glycosylation, on prostaglandin (PG) F2α-stimulated phosphoinositide (PI) hydrolysis was examined in cultured rat astrocytes. Pretreatment of cultured astrocytes with tunicamycin (25–250 ng/ml) inhibited subsequent PGF2α (1 μM)-stimulated PI hydrolysis in concentration- and time-dependent manners. The inhibition completely recovered after removal of tunicamycin and re-incubation for 12 h. Tunicamycin pretreatment (100 ng/ml for 12 h) significantly blocked [35S]methionine incorporation into cultured astrocytes, but cell viability was not affected under the condition. Inhibitors of processing of N-linked sugar chains such as bromoconduritol, 1-deoxymannojirimycin, and swainsonine had no effect on PI response to PGF2α. These observations suggest that PGF2α receptor is N-linked glycosylated.
Key WordsProstaglandin F2α receptors tunicamycin N-Linked glycosylation phosphoinositide hydrolysis astrocytes
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