Molecular mechanism of non-genomic action of ecdysone

虽然普遍认为蜕皮激素通过与核蜕皮激素受体结合发挥作用，但质膜上的其他受体作为蜕皮激素受体（mEcR），介导蜕皮激素作用，而不需要基因表达（非基因组作用）。药理学提示mEcR为G蛋白偶联受体（GPCR）。激活的GPCR激活信号转导通路，最终导致caspase 3样蛋白酶激活，诱导细胞死亡。此外，我们发现蜕皮激素对细胞死亡的作用是由非内分泌调节的。前丝腺含有葡萄糖氧化酶，该酶介导过氧化氢（H_2O_2）的产生，而H_2O_2抑制脱皮激素的作用，即细胞死亡的进展。

Although it is generally accepted thatecdysoneexerts itseffects through binding with nuclear ecdysone receptor, other receptor on plasma membrane acts as a ecdysone receptor(mEcR) that mediates ecdysone action without gene expression(non-genomic action). mEcR is suggested pharmacologically to be G protein-coupled receptor(GPCR). The activated GPCR activates the signal transduction pathway, which culminates caspase 3-like protease activation and induces cell death. In addition, we showed that ecdysone action against cell death was regulated non-endocrinologically. Anterior silk glands contain glucose oxidase that mediates production of hydrogen peroxide(H_2O_2), and H_2O_2suppresses the ecdysone action, i. e., progression of cell death.