Inhibition by ca2+ of the incorporation of myo-inositol into phosphatidylinositol

Inhibition by ca2+ of the incorporation of myo-inositol into phosphatidylinositol
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ca2 抑制肌醇掺入磷脂酰肌醇

DOI:
10.1016/0303-7207(81)90027-7
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发表时间:
1981
影响因子:
4.1
通讯作者:
B. Sacktor
B. Sacktor
中科院分区:
医学2区
文献类型:
--
作者:
Egawa Kohji;Takenawa Tadaomi;B. Sacktor

文献摘要

被引文献

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测定了肌-[2- 3 H]肌醇掺入主动脉和输精管磷脂酰肌醇的量,并测定了Ca ~(2+)和其它二价阳离子的影响。当在正常Krebs-Ringer缓冲液中孵育时,仅可忽略的放射性掺入主动脉切片中。Mn ~(2+)对土壤的掺入有显著的促进作用。增强的掺入是由于CDP-甘油二酯:肌醇转移酶活性的增加,而不是肌肌醇交换反应。在20 mM Mg 2+存在下,1 mM Mn 2+使转移酶活性增加20倍。Ca ~(2+)强烈抑制Mn ~(2+)刺激的活性。在Mn 2+的情况下,但存在20 mM Mg 2+,0.01 mM Ca 2+的转移酶活性被抑制80%。用离子载体A23187和EGTA去除组织中的内源性Ca ~(2+),可增加肌醇与磷脂酰肌醇的结合。这些结果表明,Ca ~(2+)抑制磷脂酰肌醇的合成。胆碱能和α-肾上腺素能激动剂在促进磷脂酰肌醇降解和周转以及引起Ca 2+内流方面的拟议作用应不利于细胞磷脂酰肌醇含量的恢复。
The incorporation ofmyo-[2-3H]inositol into phosphatidylinositol of the aorta and the vas deferens was measured and the effects of Ca2+and other divalent cations were determined. When incubated in normal Krebs-Ringer buffer, only negligible radioactivity was incorporated into aorta slices. Mn2+increased the incorporation greatly. The enhanced incorporation was attributable to an increase in CDP-diglyceride:inositol transferase activity, rather than themyo-inositol exchange reaction. Transferase activity was increased 20-fold by 1 mM Mn2+, in the presence of 20 mM Mg2+. The Mn2+-stimulated activity was strongly inhibited by Ca2+. In the absence of Mn2+, but presence of 20 mM Mg2+, transferase activity was inhibited 80% by 0.01 mM Ca2+. Removal of endogenous Ca2+from the tissue by ionophore A23187 and EGTA increased the incorporation ofmyo-[2-3H]inositol into phosphatidylinositol. These findings indicate that Ca2+inhibited the synthesis of phosphatidylinositol. The proposed action of cholinergic and α-adrenergic agonists in enhancing the degradation and turnover of phosphatidylinositol and in provoking the influx of Ca2+should be unfavorable to the recovery of cellular phosphatidylinositol content.