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缺乏糖蛋白IV的个体中血小板与胶原蛋白的黏附

Platelet adhesion to collagen in individuals lacking glycoprotein IV.

作者信息

McKeown L, Vail M, Williams S, Kramer W, Hansmann K, Gralnick H

机构信息

Hematology Service, National Institutes of Health, Bethesda, MD 20892.

出版信息

Blood. 1994 May 15;83(10):2866-71.

PMID:7514049
Abstract

The Naka isoantigen is expressed on glycoprotein (GP) IV (CD36), a platelet membrane GP that has been identified as having a role in platelet interactions with collagen and thrombospondin and in binding Plasmodium falciparum-infected erythrocytes to endothelial cells and melanoma cells. We have studied normal platelets and Naka- platelets from two Japanese donors that have 1% of GPIV by concentration-dependent antibody binding and flow cytometry. We studied the adherence of normal and Naka- platelets to types I, III, and IV collagen in static and to type I collagen in flowing systems at high shear force. We have also studied aggregation of normal and Naka- platelets to type I collagen. Naka- platelets showed normal or increased aggregation to type I collagen and normal adhesion to types I, III, and IV collagen in the presence of Mg++ or EDTA. Platelet aggregation and adhesion were inhibited by the anti-alpha 2 beta 1 antibody 176D7 to the same extent in Naka- as in normal platelets. We also studied endogenous thrombospondin surface expression and found that thrombin-stimulated Naka- platelets expressed the same amount of thrombospondin as did normal platelets. From our studies with Naka- platelets, we cannot identify a definitive role for GPIV in platelet aggregation, in adhesion to types I, III, and IV collagen, or in endogenous thrombospondin binding to platelets.

摘要

中抗原在糖蛋白(GP)IV(CD36)上表达,GPIV是一种血小板膜糖蛋白,已被确定在血小板与胶原蛋白和血小板反应蛋白的相互作用中,以及在恶性疟原虫感染的红细胞与内皮细胞和黑色素瘤细胞的结合中发挥作用。我们通过浓度依赖性抗体结合和流式细胞术研究了来自两名日本供体的正常血小板和中抗原阴性血小板,其GPIV含量为1%。我们研究了正常血小板和中抗原阴性血小板在静态条件下对I型、III型和IV型胶原蛋白的黏附,以及在高剪切力流动系统中对I型胶原蛋白的黏附。我们还研究了正常血小板和中抗原阴性血小板对I型胶原蛋白的聚集情况。在存在镁离子或乙二胺四乙酸(EDTA)的情况下,中抗原阴性血小板对I型胶原蛋白的聚集正常或增加,对I型、III型和IV型胶原蛋白的黏附正常。抗α2β1抗体176D7对中抗原阴性血小板和正常血小板的血小板聚集和黏附的抑制程度相同。我们还研究了内源性血小板反应蛋白的表面表达,发现凝血酶刺激的中抗原阴性血小板表达的血小板反应蛋白量与正常血小板相同。通过对中抗原阴性血小板的研究,我们无法确定GPIV在血小板聚集、对I型、III型和IV型胶原蛋白的黏附或内源性血小板反应蛋白与血小板的结合中的确切作用。

相似文献

1
Platelet adhesion to collagen in individuals lacking glycoprotein IV.缺乏糖蛋白IV的个体中血小板与胶原蛋白的黏附
Blood. 1994 May 15;83(10):2866-71.
2
Adhesive functions of platelets lacking glycoprotein IV (CD36).缺乏糖蛋白IV(CD36)的血小板的黏附功能。
Blood. 1991 Dec 1;78(11):2809-13.
3
A platelet membrane glycoprotein (GP) deficiency in healthy blood donors: Naka- platelets lack detectable GPIV (CD36).健康献血者中血小板膜糖蛋白(GP)缺乏:中血小板缺乏可检测到的GPIV(CD36)。
Blood. 1990 Nov 1;76(9):1698-703.
4
Platelet adhesion to collagen and endothelial cell matrix under flow conditions is not dependent on platelet glycoprotein IV.在流动条件下,血小板与胶原蛋白和内皮细胞基质的黏附并不依赖于血小板糖蛋白IV。
Blood. 1994 Jun 1;83(11):3240-4.
5
Platelets lacking functional CD36 (glycoprotein IV) show reduced adhesion to collagen in flowing whole blood.缺乏功能性CD36(糖蛋白IV)的血小板在流动的全血中对胶原蛋白的黏附能力降低。
Blood. 1993 Jul 15;82(2):491-6.
6
Identification of glycoprotein IV (CD36) as a primary receptor for platelet-collagen adhesion.鉴定糖蛋白IV(CD36)为血小板与胶原蛋白黏附的主要受体。
J Biol Chem. 1989 May 5;264(13):7576-83.
7
Platelet activation and inhibition of malarial cytoadherence by the anti-CD36 IgM monoclonal antibody NL07.抗CD36 IgM单克隆抗体NL07对血小板的激活作用及对疟原虫细胞黏附的抑制作用
Blood. 1993 Dec 15;82(12):3637-47.
8
Identification of the platelet-specific alloantigen, Naka, on platelet membrane glycoprotein IV.血小板膜糖蛋白IV上血小板特异性同种抗原Naka的鉴定。
Blood. 1990 Feb 1;75(3):684-7.
9
Deficiency of intact thrombospondin and membrane glycoprotein Ia in platelets with defective collagen-induced aggregation and spontaneous loss of disorder.血小板中完整的血小板反应蛋白和膜糖蛋白Ia缺乏,伴有胶原诱导聚集缺陷和无序状态的自发丧失。
Blood. 1988 Apr;71(4):1074-8.
10
Collagen induces normal signal transduction in platelets deficient in CD36 (platelet glycoprotein IV).
Thromb Haemost. 1994 Mar;71(3):353-6.

引用本文的文献

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Arterioscler Thromb Vasc Biol. 2010 Dec;30(12):2350-6. doi: 10.1161/ATVBAHA.110.207498. Epub 2010 Nov 11.
2
Platelet adhesion under flow.流动状态下的血小板黏附
Microcirculation. 2009 Jan;16(1):58-83. doi: 10.1080/10739680802651477.
3
Distinct roles of GPVI and integrin alpha(2)beta(1) in platelet shape change and aggregation induced by different collagens.糖蛋白VI(GPVI)和整合素α2β1在不同胶原蛋白诱导的血小板形状改变和聚集过程中的不同作用
Br J Pharmacol. 2002 Sep;137(1):107-17. doi: 10.1038/sj.bjp.0704834.
4
The Fc receptor gamma-chain and the tyrosine kinase Syk are essential for activation of mouse platelets by collagen.Fc受体γ链和酪氨酸激酶Syk对于胶原蛋白激活小鼠血小板至关重要。
EMBO J. 1997 May 1;16(9):2333-41. doi: 10.1093/emboj/16.9.2333.
5
Reduced uptake of oxidized low density lipoproteins in monocyte-derived macrophages from CD36-deficient subjects.CD36缺陷受试者的单核细胞衍生巨噬细胞对氧化型低密度脂蛋白的摄取减少。
J Clin Invest. 1995 Oct;96(4):1859-65. doi: 10.1172/JCI118231.