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Mastoparan-Stimulated Prolactin Secretion in Rat Pituitary GH₃ Cells Involves Activation of G_q/11 Proteins

Department of Molecular Biology (Y.Y., K.U., S.K.), The Tokyo Metropolitan Institute of Medical Science (Rinsho-ken), 3-18-22, Honkomagome Bunkyo-ku, Tokyo 113, Japan; Department of Chemistry (K.U., H.I.), Aoyama-Gakuin University, 6-16-1, Chitosedai, Setagaya-ku, Tokyo 157, Japan

Address all correspondence and requests for reprints to: Dr. Yukiko Yajima, Department of Molecular Biology, The Tokyo Metropolitan Institute of Medical Science (Rinsho-ken), 3-18-22, Honkomagome, Bunkyo-ku, Tokyo 113, Japan. E-mail: yajima{at}rinshoken.or.jp

Mastoparan has been reported to induce a wide variety of cellular actions by activating GTP-binding proteins (G proteins) in various cells. Here, we demonstrate that mastoparan is able to stimulate the secretion of PRL from rat anterior pituitary tumor GH₃ cells in dose- and time-dependent manners. Mastoparan had no effect on the accumulation of intracellular cAMP; however, it induced a rapid increase in the intracellular Ca²⁺ concentration in GH₃ cells. Extracellular Ca²⁺ was required for mastoparan-induced PRL secretion, which was inhibited by nifedipine, an L-type Ca²⁺ channel blocker. Incubation of mastoparan with myo-[³H]inositol-labeled GH₃ cells also resulted in the increased formation of inositol phosphates (InsPs) compared with control cells. Neomycin sulfate and U73122, both phospholipase C inhibitors, suppressed mastoparan-induced PRL secretion. Guanosine 5'-[ß-thio]diphosphate (GDPßS) encapsulated in GH₃ cells by reversible electropermeabilization suppressed the response to mastoparan. However, pretreatment with pertussis toxin had no effect on the stimulation of PRL secretion by mastoparan, and both Mas7 (a highly active analogue of mastoparan) and Mas17 (an inactive analogue) enhanced the secretion of PRL to a similar level to that of mastoparan-induced GH₃ cells. In contrast, the substance P-related peptide GPant-2A, a G_q antagonist, inhibited mastoparan-induced PRL release, whereas GPant-2, a G_i/o antagonist, did not in electropermeabilized GH₃ cells. Moreover, a specific G_q/11 antibody against the carboxyl terminus of the G_q/11 -subunit blocked the stimulatory effect of mastoparan on secretion and mastoparan-stimulated InsPs production in digitonin-permeabilized GH₃ cells. These results indicate that mastoparan induces the Ca²⁺-regulated secretion of PRL from GH₃ cells by activating G_q/11 and the phospholipase C pathway.

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