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首页> 外文期刊>Biochemical Pharmacology >Calcium-pH crosstalks in rat mast cells: modulation by transduction signals show non-essential role for calcium in alkaline-induced exocytosis.
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Calcium-pH crosstalks in rat mast cells: modulation by transduction signals show non-essential role for calcium in alkaline-induced exocytosis.

机译：大鼠肥大细胞中的钙pH值串扰：转导信号的调节显示钙在碱性诱导的胞吐作用中没有重要作用。

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Alkalinization of cytosolic pH with ammonium chloride (NH(4)Cl) was reported to be a stimulus for mast cell degranulation. This paper studied the modulatory role of drugs that target protein kinase C (PKC), adenosine 3',5'-cyclic monophosphate (cAMP), tyrosine kinase (TyrK) and phosphatidylinositol 3-kinase (PI(3)K) on this effect. We used Go6976 (100nM) and low concentrations of GF109203X (Gf) (50nM) to inhibit calcium-dependent PKC isozymes. For calcium-independent isozymes, we used 500nM Gf, and 10muM rottlerin to specifically inhibit PKC delta, and chelerythrine as non-specific PKC inhibitor. Genistein (10muM) and lavendustin A (1muM) were used as unspecific TyrK inhibitors, and 10nM wortmannin as a PI(3)K inhibitor. Chelerythrine and 50nM Gf inhibit histamine release in the presence of external calcium. The inhibition caused by wortmannin was strictly internal calcium-dependent. cAMP-active drugs did not modify the response to NH(4)Cl. The effect of NH(4)Cl on histamine release was triggered by a transient elevation on cytosolic pH, which was simultaneous to an elevation on cytosolic calcium and followed by a probable Ca(2+)-H(+) exchange after addition of external calcium. EGTA inhibit the response to suboptimal concentrations of NH(4)Cl, and BAPTA increased the effect of NH(4)Cl. There is a clear relationship between NH(4)Cl-mediated calcium release and histamine release, since those drugs that inhibit this release also inhibit NH(4)Cl-mediated histamine release; nevertheless, NH(4)Cl-mediated histamine release was possible in the absence of any calcium release, as shown with BAPTA. This data, in combination with the results with PKC inhibitors, suggest that calcium is not only unnecessary to trigger cell activation, but also that it may be a negative modulator of NH(4)Cl-mediated exocytosis.
机译：据报道用氯化铵（NH（4）Cl）的碱溶液pH的碱化是肥大细胞脱粒的一种刺激。本文研究了针对蛋白激酶C（PKC），腺苷3'，5'-环一磷酸（cAMP），酪氨酸激酶（TyrK）和磷脂酰肌醇3-激酶（PI（3）K）的药物的调节作用。 。我们使用Go6976（100nM）和低浓度的GF109203X（Gf）（50nM）来抑制钙依赖性PKC同工酶。对于不依赖钙的同工酶，我们使用500nM Gf和10μM的rottlerin特异性抑制PKCδ，而白屈菜红碱作为非特异性PKC抑制剂。 Genistein（10μM）和lavendustin A（1μM）被用作非特异性TyrK抑制剂，而10nM wortmannin被用作PI（3）K抑制剂。白屈菜红碱和50nM Gf在外部钙存在下抑制组胺释放。渥曼青霉素引起的抑制作用完全是内部钙依赖性的。 cAMP活性药物不会改变对NH（4）Cl的反应。 NH（4）Cl对组胺释放的影响是由细胞溶质pH的短暂升高触发的，该升高与细胞质钙的升高同时发生，随后在添加外部物质后可能发生Ca（2 +）-H（+）交换钙。 EGTA抑制对次适浓度的NH（4）Cl的响应，而BAPTA则增加了NH（4）Cl的作用。 NH（4）Cl介导的钙释放与组胺释放之间存在明显的关系，因为抑制这种释放的药物也抑制NH（4）Cl介导的组胺释放;但是，如BAPTA所示，在没有任何钙释放的情况下，NH（4）Cl介导的组胺释放是可能的。该数据与PKC抑制剂的结果相结合，表明钙不仅不仅不需要触发细胞活化，而且可能是NH（4）Cl介导的胞吐作用的负调节剂。

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