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作者Hsieh, Y.C.; Lin, P.L.;Gu, S.H.
出版日期2014
著作名稱Signaling of reactive oxygen species in PTTH-stimulated ecdysteroidogenesis in prothoracic glands of the silkworm, Bombyx mori
刊名Journal of Insect Physiology
63
頁數32-39
被收錄索引SCI
關鍵字Bombyx mori; Ca(2+); Ecdysone; PTTH; Prothoracic glands; ROS signaling
摘要Our previous study demonstrated that mitochondria-derived reactive oxygen species (ROS) generation is involved in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis by Bombyx mori prothoracic glands (PGs). In the present study, we further investigated the mechanism of ROS production and the signaling pathway mediated by ROS. PTTH-stimulated ROS production was markedly attenuated in a Ca2 -free medium. The phospholipase C (PLC) inhibitor, U73122, greatly inhibited PTTH-stimulated ROS production, indicating the involvement of Ca2 and PLC. When the PGs were treated with agents that directly elevate the intracellular Ca2 concentration (either A23187, or the protein kinase C (PKC) activator, phorbol 12-myristate acetate (PMA)), a great increase in ROS production was observed. We further investigated the action mechanism of PTTH-stimulated ROS signaling. Results showed that in the presence of either an antioxidant (N-acetylcysteine, NAC), or the mitochondrial oxidative phosphorylation inhibitors (rotenone, antimycin A, the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), and diphenylene iodonium (DPI)), PTTH-regulated phosphorylation of ERK, 4E-BP, and AMPK was blocked. Treatment with 1 mM of H2O2 alone activated the phosphorylation of ERK and 4E-BP, and inhibited AMPK phosphorylation. From these results, we conclude that PTTH-stimulated ROS signaling is Ca2 - and PLC-dependent and that ROS signaling appears to lie upstream of the phosphorylation of ERK, 4E-BP, and AMPK.
DOI10.1016/j.jinsphys.2014.02.004
系統號NO000003762

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