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C3a诱导豚鼠血小板活化及刺激特异性可逆脱敏。

C3a induced activation and stimulus specific reversible desensitization of guinea pig platelets.

作者信息

Zanker B, Rasokat H, Hadding U, Bitter-Suermann D

出版信息

Agents Actions Suppl. 1982;11:147-57.

PMID:6983827
Abstract

C3a and its C-terminal hexapeptide lead to a dose dependent release of biogenic amines and nucleotides stored in platelet's granules. The release reaction can be measured by tritiated serotonin or by ATP, indicated by an ATP specific bioluminescence assay. We tested the capability of C3a to induce aggregation of washed platelets. The recently described phenomenon of low dose, stimulus specific desensitization of platelets to the anaphylatoxic peptides C3a and C5a could be shown by measuring the release reaction as well as the aggregation. Further we could demonstrate the reversibility of the stimulus specific desensitization within 2 to 3 hours. The desensitization was proven to be temperature dependent. The recovery of function was independent of newly synthetized protein and is discussed as the result of receptor-recycling.

摘要

C3a及其C末端六肽可导致血小板颗粒中储存的生物胺和核苷酸呈剂量依赖性释放。释放反应可用氚标记的血清素或ATP来测量,ATP特异性生物发光测定法可对此进行指示。我们测试了C3a诱导洗涤后血小板聚集的能力。通过测量释放反应以及聚集情况,可以证明最近描述的低剂量、刺激特异性血小板对过敏毒素肽C3a和C5a脱敏的现象。此外,我们还能证明刺激特异性脱敏在2至3小时内具有可逆性。已证实脱敏与温度有关。功能的恢复与新合成的蛋白质无关,被认为是受体再循环的结果。

相似文献

1
C3a induced activation and stimulus specific reversible desensitization of guinea pig platelets.C3a诱导豚鼠血小板活化及刺激特异性可逆脱敏。
Agents Actions Suppl. 1982;11:147-57.
2
Platelet-serotonin release by C3a and C5a: two independent pathways of activation.C3a和C5a诱导的血小板-血清素释放:两条独立的激活途径
J Immunol. 1981 Apr;126(4):1506-9.
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J Immunol. 1988 May 15;140(10):3496-501.
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Comparative study on biological activities of various anaphylatoxins (C4a, C3a, C5a). Investigations on their ability to induce platelet secretion.各种过敏毒素(C4a、C3a、C5a)生物活性的比较研究。关于它们诱导血小板分泌能力的研究。
Inflammation. 1981 Dec;5(4):263-73. doi: 10.1007/BF00911092.
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Induction of thromboxane release from macrophages by anaphylatoxic peptide C3a of complement and synthetic hexapeptide C3a 72-77.补体过敏毒素肽C3a和合成六肽C3a 72-77诱导巨噬细胞释放血栓素
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Low zone desensitization: a stimulus-specific control mechanism of cell response. Investigations on anaphylatoxin-induced platelet secretion.低区脱敏:细胞反应的一种刺激特异性控制机制。关于过敏毒素诱导血小板分泌的研究。
J Exp Med. 1982 Mar 1;155(3):698-710. doi: 10.1084/jem.155.3.698.
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Induction of platelet aggregation by the complement-derived peptides C3a and C5a.补体衍生肽C3a和C5a诱导血小板聚集。
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Synthetic C3a analogs as specific inhibitors of C3a activity.
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Demonstration of high-affinity binding sites for C3a anaphylatoxin on guinea-pig platelets.豚鼠血小板上C3a过敏毒素高亲和力结合位点的证明。
Scand J Immunol. 1978;8(6):551-5. doi: 10.1111/j.1365-3083.1978.tb00555.x.

引用本文的文献

1
Inflammatory mediators released by complement-derived peptides.补体衍生肽释放的炎症介质。
Agents Actions. 1983 Aug;13(5-6):405-14. doi: 10.1007/BF02176403.
2
Design and biological activity of a new generation of synthetic C3a analogues by combination of peptidic and non-peptidic elements.通过肽类和非肽类元素组合设计新一代合成C3a类似物及其生物活性
Biochem J. 1988 Oct 1;255(1):209-16.
3
Functional activities of synthetic anaphylatoxic peptides in widely used biological assays.合成过敏毒素肽在广泛使用的生物学检测中的功能活性。
Clin Exp Immunol. 1992 May;88(2):368-72. doi: 10.1111/j.1365-2249.1992.tb03090.x.