Elevation of inositol tetrakisphosphate parallels inhibition of Ca(2+)-dependent Cl- secretion in T84 cells.
Elevation of inositol tetrakisphosphate parallels inhibition of Ca(2+)-dependent Cl- secretion in T84 cells.
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四磷酸肌醇的升高与T84细胞中Ca(2)依赖性Cl-分泌的抑制平行。
DOI：
10.1152/ajpcell.1993.264.3.c671
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Traynor-Kaplan,AE
中科院分区：
文献类型：
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作者：
Kachintorn,U;Vajanaphanich,M;Barrett,KE;Traynor-Kaplan,AE
甲胆碱和组胺都能刺激结肠上皮细胞系T84中钙依赖性氯离子的分泌。然而，用恰巴醇预处理细胞单层可阻断随后由塔塔sigargin诱导的氯离子分泌，但不能阻断该药物刺激的钙离子升高，而组胺预处理既不能阻断塔塔sigargin诱导的氯离子分泌，也不能阻断钙离子升高。为了检验肌醇磷酸代谢是否能解释这种差异，我们测量了细胞刺激后放射性标记肌醇磷酸的水平：Ins(1,3,4)P3、Ins(1,4,5)P3、Ins(1,3,4,5)P4、Ins-(1,3,4,6)P4、Ins(3,4,5,6)P4、InsP5和InsP6。虽然在5 s时卡巴甘醇和组胺均增加Ins(1,4,5)P3，但在卡巴甘醇作用后较晚的时间点Ins(1,3,4)P3和InsP4水平的增加比组胺更大且更持久，这与氯离子分泌反应的抑制相对应。
Carbachol and histamine both stimulate calcium-dependent chloride secretion in the colonic epithelial cell line, T84. However, pretreatment of cell monolayers with carbachol blocks subsequent chloride secretion induced by thapsigargin but not the calcium elevation stimulated by this agent, whereas histamine pretreatment blocks neither thapsigargin-induced chloride secretion nor calcium elevation. To examine whether inositol phosphate metabolism might account for this difference, we measured levels of radiolabeled inositol phosphates: Ins(1,3,4)P3, Ins(1,4,5)P3, Ins(1,3,4,5)P4, Ins-(1,3,4,6)P4, Ins(3,4,5,6)P4, InsP5, and InsP6 after cell stimulation. Although both carbachol and histamine increase Ins (1,4,5)P3 at 5 s, there is a greater and more persistent increase in the levels of Ins(1,3,4)P3 and InsP4 at later time points after carbachol than histamine, which corresponded to the suppression of the chloride secretory response.