Wijelath E S, Kardasz A M, Drummond R, Watson J
Division of Biochemistry, University of Strathclyde, Glasgow.
Biochem Biophys Res Commun. 1988 Apr 15;152(1):392-7. doi: 10.1016/s0006-291x(88)80726-5.
Stimulation of mouse peritoneal macrophages by Interleukin-one (IL-1) provoked rapid increases in the levels of inositol mono, bis, tris and tetrakisphosphates (IP1, IP2, IP3 and IP4 respectively). IP3 was by far the major metabolite formed and time course studies revealed that IP2 and IP3 were formed more rapidly than IP1 and IP4 in response to IL-1 stimulation. The IP2 and IP3 levels peaked at five seconds while there was a time lag of five seconds in the IP4 response and the IP1 levels increased relatively steadily over the time course of the experiments. Levels of IP2, IP3 and IP4 all returned almost to control levels by 60s. The rapid formation of the inositol phosphate metabolites was concomitant with a decrease (84%) in the levels of phosphatidyl-inositol 4,5-bisphosphate (PIP2) in the macrophages. These results suggest that the mechanism of IL-1 receptor activation is by the rapid hydrolysis of phosphoinositides and generation of the second messenger IP3.
白细胞介素 - 1（IL - 1）刺激小鼠腹腔巨噬细胞后，肌醇单磷酸、双磷酸、三磷酸和四磷酸（分别为IP1、IP2、IP3和IP4）水平迅速升高。IP3是迄今为止形成的主要代谢产物，时间进程研究表明，响应IL - 1刺激时，IP2和IP3的形成比IP1和IP4更快。IP2和IP3水平在5秒时达到峰值，而IP4的响应有5秒的时间延迟，并且在实验的时间进程中IP1水平相对稳定地增加。到60秒时，IP2、IP3和IP4的水平几乎都恢复到对照水平。肌醇磷酸代谢产物的快速形成与巨噬细胞中磷脂酰肌醇4,5 - 二磷酸（PIP2）水平的降低（84%）同时发生。这些结果表明，IL - 1受体激活的机制是磷酸肌醇的快速水解和第二信使IP3的生成。
