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氟化铝和磷酸酶抑制剂对大鼠腮腺腺泡细胞中Na(+)-K(+)-2Cl-协同转运体的激活作用。

Activation of the Na(+)-K(+)-2Cl- cotransporter in rat parotid acinar cells by aluminum fluoride and phosphatase inhibitors.

作者信息

Paulais M, Turner R J

机构信息

Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

J Biol Chem. 1992 Oct 25;267(30):21558-63.

PMID:1383225
Abstract

The bumetanide-sensitive component of pHi recovery from an NH4Cl-induced acute alkaline load was used as a measure of Na(+)-K(+)-2Cl- cotransport activity in rat parotid acini. Acinar treatment with NaF/AlCl3 (15 mM NaF plus 10 microM AlCl3) induced a 5-fold stimulation in the initial rate of bumetanide-sensitive pHi recovery. This effect was dependent on NaF concentration (K1/2 approximately 7 mM) and was blunted in the presence of the Al3+ chelator desferal mesylate suggesting that it might be due to the aluminofluoride ion, AlF-4. NaF/AlCl3 treatment did not increase acinar intracellular cAMP levels but did result in an increase in intracellular calcium concentration (from 87 +/- 5 to 181 +/- 2 nM) and in acinar cell shrinkage (12 +/- 1%). But the stimulation of the Na(+)-K(+)-2Cl- cotransporter by NaF/AlCl3 persisted in acini which had been depleted of their intracellular Ca2+ stores. In these acini no effect of NaF/AlCl3 on intracellular calcium or cell volume was observed, indicating that stimulation of the cotransporter was not secondary to either of these phenomena. The effect of NaF/AlCl3 on the cotransporter was blocked by the protein kinase inhibitor K252a indicating the involvement of a protein phosphorylation event. This result is consistent with either NaF/AlCl3-dependent protein kinase activation or phosphatase inhibition. The stimulation of the cotransporter by NaF/AlCl3 was mimicked by the protein phosphatase inhibitor calyculin A; however, this effect was not blocked by K252a suggesting that a different protein kinase from that associated with NaF/AlCl3 may be involved. The data indicate that the Na(+)-K(+)-2Cl- cotransporter in this tissue is under tight regulatory control, in all likelihood via multiple protein kinase/phosphatase systems. The physiological roles of these regulatory events in modulating acinar fluid secretion driven by the Na(+)-K(+)-2Cl- cotransporter remain to be elucidated.

摘要

用氯化铵诱导急性碱性负荷后细胞内pH值(pHi)恢复中对布美他尼敏感的部分作为大鼠腮腺腺泡中Na(+)-K(+)-2Cl-协同转运活性的指标。用NaF/AlCl3(15 mM NaF加10 μM AlCl3)处理腺泡,可使布美他尼敏感的pHi恢复初始速率提高5倍。这种效应依赖于NaF浓度(半最大效应浓度约为7 mM),且在存在Al3+螯合剂甲磺酸去铁胺的情况下减弱,提示可能是由于铝氟离子AlF-4所致。NaF/AlCl3处理并未增加腺泡细胞内cAMP水平,但确实导致细胞内钙浓度升高(从87±5 nM升至181±2 nM)以及腺泡细胞皱缩(12±1%)。然而,NaF/AlCl3对Na(+)-K(+)-2Cl-协同转运体的刺激在细胞内Ca2+储存已耗尽的腺泡中仍然存在。在这些腺泡中未观察到NaF/AlCl3对细胞内钙或细胞体积的影响,表明对协同转运体的刺激并非继发于这些现象中的任何一种。蛋白激酶抑制剂K252a可阻断NaF/AlCl3对协同转运体的作用,表明涉及蛋白磷酸化事件。这一结果与NaF/AlCl3依赖性蛋白激酶激活或磷酸酶抑制一致。蛋白磷酸酶抑制剂煅房蛤素A可模拟NaF/AlCl3对协同转运体的刺激;然而,这种效应未被K252a阻断,提示可能涉及与NaF/AlCl3相关的不同蛋白激酶。数据表明该组织中的Na(+)-K(+)-2Cl-协同转运体受到严格的调控,很可能是通过多种蛋白激酶/磷酸酶系统。这些调控事件在调节由Na(+)-K(+)-2Cl-协同转运体驱动的腺泡液体分泌中的生理作用仍有待阐明。

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