TNF‐α stimulates increased plasma membrane guanine nucleotide binding protein activity in polymorphonuclear leukocytes
TNF‐α stimulates increased plasma membrane guanine nucleotide binding protein activity in polymorphonuclear leukocytes
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TNF-α 刺激多形核白细胞质膜鸟嘌呤核苷酸结合蛋白活性增加
DOI：
--
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发表时间：
1995
影响因子：
5.5
通讯作者：
K. Mcleish
中科院分区：
文献类型：
--
作者：
J. Klein;J. Scherzer;G. Harding;A. Jacobs;K. Mcleish
TNF-α增强了多形核白细胞（PMN）对化学引诱物的反应：然而，其发生机制尚不清楚。我们使用fMLP作为模型趋化因子，阐明了TNF-α通过增加趋化因子受体跨膜信号转导增强PMN对趋化因子的反应的假设。与来自对照细胞（CM）的膜相比，在从暴露于TNF-α 100 U/ml 10分钟（TNF-M）的PMN分离的质膜中，fMLP刺激的鸟嘌呤核苷酸结合（G）蛋白活化显著增加。CM和TNF-M中甲酰肽受体数量和亲和力无显著差异。分别通过百日咳毒素和霍乱毒素（CT）催化的ADP-核糖基化测定，TNF-M中Gi和G3含量增加。增加的Gi与甲酰基肽受体偶联，如Gi的受体特异性CT标记所示。免疫印迹分析显示TNF-M中Gαi2和Gα3均增加。TNF-α处理的PMN中NaF刺激的磷脂酶D活性增加证明了G蛋白含量增加的功能活性。我们得出结论，TNF-α快速刺激PMN质膜G蛋白表达增加，G蛋白将甲酰肽受体与效应酶偶联。G蛋白表达的调节可能是TNF调节PMN功能的重要机制。J.利瓦克57：500-506; 1995.
TNF‐α enhances the response of polymorphonuclear leukocytes (PMN) to chemoattractants: however, the mechanism by which this occurs is unclear. We addressed the hypothesis that TNF‐α enhances the PMN response to chemoattractants by increasing chemoattractant receptor transmembrane signaling, using fMLP as the model chemoattractant. fMLP‐stimulated guanine nucleotide binding (G) protein activation was significantly increased in plasma membranes isolated from PMNs exposed to TNF‐α 100 U/ml for 10 minutes (TNF‐M), compared to membranes from control cells (CM). Formyl peptide receptor number and affinity were not significantly different in CM and TNF‐M. Gi and G3 content were increased in TNF‐M as measured by pertussis toxin and cholera toxin (CT) catalyzed ADP‐ribosylation, respectively. The increased Gi was coupled to the formyl peptide receptor as shown by receptor‐specific CT labeling of Gi. Immunoblot analysis showed that both Gαi2 and Gα3 were increased in TNF‐M. The functional activity of the increased G protein content was demonstrated by increased NaF‐stimulated phospholipase D activity in TNF‐α‐treated PMNs. We conclude that TNF‐α rapidly stimulates increased PMN plasma membrane expression of G proteins that couple formyl peptide receptors to effector enzymes. Regulation of G protein expression may be a significant mechanism by which TNF regulates PMN function. J. Leukoc. Biol. 57: 500–506; 1995.
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DOI：
--
发表时间：
1987
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Perussia,B;Kobayashi,M;Rossi,ME;Anegon,I;Trinchieri,G
通讯作者：
Trinchieri,G
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DOI：
--
发表时间：
1985
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Smith,CD;Lane,BC;Kusaka,I;Verghese,MW;Snyderman,R
通讯作者：
Snyderman,R
脂多糖和血清导致 G 蛋白易位至细胞膜并通过 CD14 启动中性粒细胞。
DOI：
10.1016/s0006-291x(05)80329-8
发表时间：
1992
影响因子：
3.1
作者：
Yasui,K;Becker,EL;Sha'afi,RI
通讯作者：
Sha'afi,RI
影响因子：
4.4
作者：
S. Klebanoff;M. Vadas;J. Harlan;L. Sparks;J. Gamble;J. Agosti;A. Waltersdorph
通讯作者：
S. Klebanoff;M. Vadas;J. Harlan;L. Sparks;J. Gamble;J. Agosti;A. Waltersdorph
DOI：
10.1016/s0021-9258(18)77181-0
发表时间：
1990-09
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
J. Hadcock;M. Ros;D. C. Watkins;C. Malbon
通讯作者：
J. Hadcock;M. Ros;D. C. Watkins;C. Malbon