Akerman K E, Näsman J, Lund P E, Shariatmadari R, Kukkonen J P
Department of Physiology, Uppsala University, BMC, Sweden.
FEBS Lett. 1998 Jul 3;430(3):209-12. doi: 10.1016/s0014-5793(98)00664-4.
Many receptors coupled to inhibitory Go/Gi-type G proteins often also produce stimulatory signals like Ca2+ mobilisation. When expressed in CHO cells the alpha2-adrenoceptor subtypes alpha2A, alpha2B and alpkha2C mobilised Ca2+. These responses were strongly reduced by the P2Y-purinoceptor antagonist suramin. A large proportion of the total pool of purine nucleotides was found extracellularly. Removal of extracellular nucleotides with apyrase or by constant perfusion had a similar effect as suramin. These treatments did not affect the alpha2-adrenoceptor-mediated inhibition of cAMP production. This indicates that cells may be primed or their signaling pathways redirected towards Ca2+ mobilisation by 'autocrine' release of nucleotides.
许多与抑制性Go/Gi型G蛋白偶联的受体通常也会产生诸如Ca2+动员等刺激性信号。当在CHO细胞中表达时,α2 - 肾上腺素能受体亚型α2A、α2B和α2C会动员Ca2+。这些反应被P2Y - 嘌呤受体拮抗剂苏拉明强烈减弱。发现很大一部分嘌呤核苷酸池存在于细胞外。用 apyrase去除细胞外核苷酸或通过持续灌注产生的效果与苏拉明相似。这些处理并不影响α2 - 肾上腺素能受体介导的cAMP生成的抑制作用。这表明细胞可能通过核苷酸的“自分泌”释放而被启动,或者其信号通路被重定向至Ca2+动员。