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糖尿病患者血小板的膜流动性降低和膜蛋白糖基化增加与血小板对糖化胶原蛋白的粘附增加无关。

Reduced membrane fluidity and increased glycation of membrane proteins of platelets from diabetic subjects are not associated with increased platelet adherence to glycated collagen.

作者信息

Winocour P D, Watala C, Kinlough-Rathbone R L

机构信息

Department of Pathology, McMaster University, Hamilton, Ontario, Canada.

出版信息

J Lab Clin Med. 1992 Dec;120(6):921-8.

PMID:1453113
Abstract

Platelets could contribute to vascular disease in diabetes through enhanced adherence to collagen exposed in injured vessels. Increased platelet adherence to collagen in diabetes could result from an alteration in platelets and/or platelet hypersensitivity to collagen that has been glycated to a greater extent. In this study, the adherence of platelets from diabetic or control subjects to glycated or nonglycated collagen coated onto glass surfaces was examined. Membrane fluidity of platelets was also determined, since decreased membrane fluidity associated with increased glycation of membrane proteins of platelets from diabetic subjects was shown in a previous study, and decreases in membrane fluidity have been shown by others to increase platelet adhesion. Thirteen diabetic subjects were compared with 13 age-and sex-matched control subjects. Collagen was glycated (9.7 nmol glucose/mg protein) by preincubation for 12 days in glucose-rich medium (500 mmol/L). A control solution of collagen incubated without glucose for the same time had 3.3 nmol glucose/mg protein. There were no differences in the adherence of platelets from diabetic and control subjects to nonglycated and glycated collagen-coated glass. The mean steady-state fluorescence polarization value (0.187 +/- 0.002) in 1.6-diphenyl-1,3,5-hexatriene-labeled platelets from diabetic subjects was significantly greater than in platelets from control subjects (0.174 +/- 0.002, p < 0.002); thus membrane fluidity in platelets from the group of diabetic subjects was decreased. The extent of glycation of membrane proteins from diabetic subjects (25.4 +/- 0.5 nmol glucose/mg protein) was significantly greater than from control subjects (20.2 +/- 0.4 nmol glucose/mg protein, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

血小板可能通过增强对受损血管中暴露的胶原蛋白的黏附作用,在糖尿病血管疾病中发挥作用。糖尿病患者血小板对胶原蛋白的黏附增加,可能是由于血小板的改变和/或血小板对糖化程度更高的胶原蛋白超敏所致。在本研究中,检测了糖尿病患者或对照受试者的血小板对包被在玻璃表面的糖化或未糖化胶原蛋白的黏附情况。还测定了血小板的膜流动性,因为先前的一项研究表明,糖尿病患者血小板膜流动性降低与膜蛋白糖化增加有关,而其他人的研究表明膜流动性降低会增加血小板黏附。将13名糖尿病受试者与13名年龄和性别匹配的对照受试者进行比较。胶原蛋白在富含葡萄糖的培养基(500 mmol/L)中预孵育12天进行糖化(9.7 nmol葡萄糖/毫克蛋白质)。在无葡萄糖的情况下孵育相同时间的胶原蛋白对照溶液含有3.3 nmol葡萄糖/毫克蛋白质。糖尿病患者和对照受试者的血小板对未糖化和糖化胶原蛋白包被玻璃的黏附没有差异。糖尿病受试者用1,6-二苯基-1,3,5-己三烯标记的血小板的平均稳态荧光偏振值(0.187±0.002)显著高于对照受试者的血小板(0.174±0.002,p<0.002);因此,糖尿病组受试者血小板的膜流动性降低。糖尿病受试者膜蛋白的糖化程度(25.4±0.5 nmol葡萄糖/毫克蛋白质)显著高于对照受试者(20.2±0.4 nmol葡萄糖/毫克蛋白质,p<0.001)。(摘要截短于250字)

相似文献

1
Reduced membrane fluidity and increased glycation of membrane proteins of platelets from diabetic subjects are not associated with increased platelet adherence to glycated collagen.糖尿病患者血小板的膜流动性降低和膜蛋白糖基化增加与血小板对糖化胶原蛋白的粘附增加无关。
J Lab Clin Med. 1992 Dec;120(6):921-8.
2
Decreased platelet membrane fluidity due to glycation or acetylation of membrane proteins.由于膜蛋白糖基化或乙酰化导致血小板膜流动性降低。
Thromb Haemost. 1992 Nov 10;68(5):577-82.
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Diabetes mellitus alters the effect of peptide and protein ligands on membrane fluidity of blood platelets.糖尿病会改变肽和蛋白质配体对血小板膜流动性的影响。
Thromb Haemost. 1996 Jan;75(1):147-53.
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Membrane fluidity is related to the extent of glycation of proteins, but not to alterations in the cholesterol to phospholipid molar ratio in isolated platelet membranes from diabetic and control subjects.膜流动性与蛋白质糖基化程度有关,但与糖尿病患者和对照受试者分离的血小板膜中胆固醇与磷脂摩尔比的改变无关。
Thromb Haemost. 1992 May 4;67(5):567-71.
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Does reduced membrane lipid fluidity underlie the altered thrombin-induced expression of integrin α(IIb)β(3) and PADGEM-140 in membranes of platelets from diabetic juveniles?膜脂流动性降低是否是导致糖尿病青少年血小板中凝血酶诱导整合素 α(IIb)β(3)和 PADGEM-140 表达改变的原因?
Platelets. 1996;7(3):173-80. doi: 10.3109/09537109609023577.
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Pathways responsible for platelet hypersensitivity in rats with diabetes. I. Streptozocin-induced diabetes.糖尿病大鼠血小板超敏反应的相关通路。I. 链脲佐菌素诱导的糖尿病。
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Reduced membrane fluidity in platelets from diabetic patients.糖尿病患者血小板中膜流动性降低。
Diabetes. 1990 Feb;39(2):241-4. doi: 10.2337/diab.39.2.241.
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Platelet adhesion.血小板黏附
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Pathways responsible for platelet hypersensitivity in rats with diabetes. II. Spontaneous diabetes in BB Wistar rats.糖尿病大鼠血小板超敏反应的相关通路。II. BB 威斯塔大鼠的自发性糖尿病。
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[Role of nonenzymatic glycosylation of proteins in disorders of erythrocytes and blood platelets in diabetes mellitus].
Acta Haematol Pol. 1993;24(2):95-101.

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Diabetes and Hyperglycemia Affect Platelet GPIIIa Expression. Effects on Adhesion Potential of Blood Platelets from Diabetic Patients under In Vitro Flow Conditions.糖尿病和高血糖会影响血小板 GPIIIa 的表达。在体外流动条件下,对糖尿病患者血小板黏附潜力的影响。
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