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首页> 外文期刊>Cardiovascular & hematological disorders drug targets >Peptides derived from platelet non-integrin collagen-receptors or types I and III collagen inhibit collagen-platelet interaction.
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Peptides derived from platelet non-integrin collagen-receptors or types I and III collagen inhibit collagen-platelet interaction.

机译：源自血小板非整联蛋白胶原受体或I型和III型胶原的肽可抑制胶原-血小板相互作用。

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摘要

Platelet-collagen interaction plays an important role in hemostasis and pathological thrombosis. Upon an injury to the subendothelium of a blood vessel wall, platelets adhere to the denuded substrate, aggregate, and release biological substances. Many investigators have explored the use of blocking agents to interrupt the final step of binding fibrinogen on glycoprotein (GP) IIb/IIIa of activated platelets. A potent peptide is Arg-Gly-Asp-Ser (RGDS) and its derivatives in various forms. Results from many clinical trials show that the efficacy of these antagonists does not lie in blocking the adhesion of platelets to the distal site(s) of the injury as expected. Because type I and type III collagens are predominant components of blood vessel walls, other laboratories and ours have defined various active peptides from either collagen molecules or platelets as useful for blocking collagen-platelet interaction. An active hybrid peptide derived from both platelet types I and type III collagen receptors thatabolishes type I and type III collagen-induced platelet aggregation has been obtained. The hybrid peptide inhibits the binding of type I and type III collagens to washed human platelets, platelet aggregation, and the adhesion of washed platelets to rabbit aortic segments. However, the usefulness of the defined hybrid peptide in preventing thrombi formation in vivo requires further investigation.
机译：血小板胶原相互作用在止血和病理性血栓形成中起重要作用。血管壁的内皮下层受到损伤后，血小板粘附到裸露的基质上，聚集并释放生物物质。许多研究人员已经探索了使用阻断剂来中断纤维蛋白原与活化血小板糖蛋白（GP）IIb / IIIa结合的最终步骤。有效的肽是各种形式的Arg-Gly-Asp-Ser（RGDS）及其衍生物。许多临床试验的结果表明，这些拮抗剂的功效并不像预期的那样在于阻止血小板粘附至损伤的远端。由于I型和III型胶原蛋白是血管壁的主要成分，其他实验室和我们的实验室已从胶原蛋白分子或血小板中定义了各种活性肽，可用于阻断胶原蛋白与血小板的相互作用。已经获得了源自血小板I型和III型胶原受体的活性杂合肽，其消除了I型和III型胶原诱导的血小板聚集。杂合肽抑制I型和III型胶原蛋白与洗涤后的人血小板的结合，血小板聚集以及洗涤后的血小板与兔主动脉节段的粘附。但是，确定的杂合肽在预防体内血栓形成中的有用性需要进一步研究。

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