Regulation of inositol phosphate levels by prostaglandins in cultured endometrial cells.
Regulation of inositol phosphate levels by prostaglandins in cultured endometrial cells.
复制标题
培养的子宫内膜细胞中前列腺素对磷酸肌醇水平的调节。
DOI：
10.1002/jcp.1041280116
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发表时间：
1986
影响因子：
5.6
通讯作者：
Gerschenson,LE
中科院分区：
文献类型：
--
作者：
Orlicky,DJ;Silio,M;Williams,C;Gordon,J;Gerschenson,LE
用兔子宫内膜细胞培养增殖因子前列腺素F2α(PgF2α)刺激培养的兔子宫内膜细胞，可使经[3 H]-肌醇标记的细胞内[3 H]-肌醇三磷酸(IP3)、[3 H]-肌醇二磷酸(IP2)和[3 H]-肌醇一磷酸(IP1)水平迅速升高。肌醇磷酸水平在短至30s的刺激时间内即可检测到，在1 1/2−2min时达到最大值，在6~10min时降至对照水平。这种刺激呈剂量依赖关系，在10−、6M、PGF_2、α附近最大。胆碱能药物卡巴胆碱也导致IP3的时间和剂量依赖性增加。锂、镉、银、铜和锌离子对IP3的分解和IP1的积累都没有影响。相反，10−6或10−5M的钒酸盐确实导致IP1的分解减少，IP1、IP2和IP3的相应增加。前人已发现前列腺素F_2α可诱导兔子宫内膜细胞DNA合成增加，而前列腺素E_1(PGE_1)可抑制其合成。PGE_1以剂量依赖的方式抑制PGF_2α在刺激后1 1/2分钟引起的IP3升高。在cAMP和cGMP水平、细胞~(45)Ca摄取和细胞~(22)Na摄取方面，PgF_2α处理组和对照培养组无明显差异。我们推测，IP3可能是增殖剂PGF2α处理兔子宫内膜细胞后合成的细胞内信使(S)之一，它可能与cAMP一起在生长调节中发挥重要作用。
Stimulation of cultured rabbit endometrial cells by one of the rabbit endometrial cell culture proliferation factors, prostaglandin F2α(PGF2α), resulted in a very rapid increase in the intracellular levels of [3H]‐inositol triphosphate (IP3), [3H]‐inositol biphosphate (IP2), and [3H]‐inositol monophosphate (IP1) in cells prelabeled with [3H]‐inositol. These increases in inositol phosphate levels were detected in periods of stimulation as short as 30 seconds, reached a maximum by 1 1/2−2 min and declined to control levels by 6–10 min. The stimulation was dose‐dependent with maximal increases observed near 10−6M PGF2α. The cholinergic agent, carbachol, also led to time and dose‐independent increases in IP3. Lithium, cadmium, silver, copper, and zinc ions had no effect either on the breakdown of IP3or on the accumulation of IP1. In contrast, vanadate at 10−6or 10−5M did lead to a decrease in the breakdown of IP1and a concomitant increase in IP1, IP2, and IP3. PGF2αwas found previously to induce an increase in rabbit endometrial cell DNA synthesis which was inhibited by concomitant or prior addition of prostaglandin E1(PGE1). PGE1, in a dose‐dependent manner, was found to inhibit the observed IP3increase by PGF2αat 1 1/2 min of stimulation. PGF2αtreated and control cultures did not differ in cAMP or cGMP levels, cellular45Ca uptake, nor cellular22Na uptake. We propose that IP3may be one of the intracellular messenger(s) synthesized following the treatment of rabbit endometrial cell cultures with the proliferation agent PGF2αand that it may play a crucial role with cAMP in growth regulation.