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首页> 外文期刊>Cell motility and the cytoskeleton >Products of phosphoinositide specific phospholipase C can trigger dephosphorylation of cofilin in chemoattractant stimulated neutrophils.
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Products of phosphoinositide specific phospholipase C can trigger dephosphorylation of cofilin in chemoattractant stimulated neutrophils.

机译：磷酸肌醇特异性磷脂酶C的产物可触发趋化因子刺激的嗜中性粒细胞中cofilin的去磷酸化。

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摘要

The signal transduction pathways that trigger dephosphorylation of cofilin in neutrophils stimulated with the chemoattractant fMet-Leu-Phe (fMLP) were investigated with a phospho-specific antibody that recognized cofilin only when this protein was phosphorylated on ser-3. Unlike earlier studies that monitored changes in (32)P-labeled cofilin, this Ab allowed us to monitor changes in the total mass of phosphorylated cofilin during neutrophil stimulation. Neutrophils stimulated with fMLP (1.0 microM) for 1.0 min exhibited a massive loss (> 85%) of phosphate from cofilin, which was blocked by an antagonist of phosphoinositide-specific phospholipase C (PI-PLC) (1.0 microM U73122). Products of PI-PLC, sn-1,2-diglyceride and inositol (1,4,5)-trisphosphate, are known to activate protein kinase C (PKC) and increase intracellular Ca(2+), respectively. Treatment of neutrophils with agents that selectively activate PKC [4beta-phorbol 12-myristate 13-acetate (PMA) ] or cellular Ca(2+) (ionophore A23187) also triggered dephosphorylation of cofilin. Both a nonspecific (100 nM staurosporine) and a highly selective antagonist of PKC (200 nM bisindolylmaleimide I) blocked dephosphorylation of cofilin in neutrophils stimulated with PMA but not with fMLP or ionophore A23187. The calmodulin (CaM) antagonists trifluoperazine (15 microM) and W-7 (50 microM) blocked dephosphorylation of cofilin in stimulated neutrophils whereas inactive/less-active analogs of these inhibitors (15 microM promethazine, 50 microM W-5) were substantially less effective. Calyculin A (40 nM), an antagonist of type 1 and 2A protein phosphatases, also triggered a massive dephosphorylation of cofilin in unstimulated neutrophils through a pathway that was insensitive to inhibitors of type 2B phosphatases. These data suggest that both PKC-dependent and independent pathways can trigger dephosphorylation of cofilin in neutrophils with the latter pathway predominating in fMLP-stimulated cells. These pathways may also contain CaM and a type 2C and/or novel phosphatase (e.g., slingshot).
机译：用磷酸特异性抗体研究了在趋化因子fMet-Leu-Phe（fMLP）刺激下在嗜中性粒细胞中触发cofilin去磷酸化的信号转导途径，该抗体仅在该蛋白质在ser-3上被磷酸化时才识别cofilin。与早期的研究监测（32）P标记的cofilin的变化不同，这种Ab使我们能够监测嗜中性粒细胞刺激过程中磷酸化cofilin的总质量的变化。用fMLP（1.0 microM）刺激1.0分钟的嗜中性粒细胞从cofilin磷酸中大量丢失（> 85％），这被磷酸肌醇特异性磷脂酶C（PI-PLC）的拮抗剂（1.0 microM U73122）阻断。 PI-PLC，sn-1,2-甘油二酸酯和肌醇（1,4,5）-三磷酸酯的产品已知分别激活蛋白激酶C（PKC）和增加细胞内Ca（2+）。用选择性激活PKC [4β-佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）]或细胞Ca（2+）（离子载体A23187）的药物治疗中性粒细胞也触发了cofilin的去磷酸化。非特异性（100 nM星形孢菌素）和高度选择性的PKC拮抗剂（200 nM双吲哚基马来酰亚胺I）均能阻断PMA刺激的嗜中性粒细胞中cofilin的去磷酸化作用，但不能阻止fMLP或离子载体A23187刺激。钙调蛋白（CaM）拮抗剂三氟哌嗪（15 microM）和W-7（50 microM）在刺激的嗜中性粒细胞中阻断了cofilin的去磷酸化，而这些抑制剂的无活性/低活性类似物（15 microM异丙嗪，50 microM W-5）要少得多有效。 Calyculin A（40 nM）是1型和2A型蛋白磷酸酶的拮抗剂，它还通过对2B型磷酸酶抑制剂不敏感的途径触发了未刺激中性粒细胞中cofilin的大量去磷酸化。这些数据表明，PKC依赖性和独立途径均可以触发嗜中性粒细胞中cofilin的去磷酸化，后者在fMLP刺激的细胞中占主导。这些途径也可能包含CaM和2C型和/或新型磷酸酶（例如，弹弓）。

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