Do platelet apoptosis, activation, aggregation, lipid peroxidation and platelet–leukocyte aggregate formation occur simultaneously in hyperlipidemia?

Şener, Azize; Özsavcı, Derya; Oba, Rabia; Demirel, Gülderen Yanikkaya; Uras, Fi̇kri̇ye; Yardımcı, K. Turay

doi:10.1016/j.clinbiochem.2005.09.005

Cited by 44 publications

(38 citation statements)

References 37 publications

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“…Lipid peroxidation of membranes induced by reactive oxygen species alters the structure and function of membrane components followed by the platelet signaling pathway activation. Additionally, although platelets are anucleated cells, apoptosis like events take place both in vivo and in vitro and they can also synthesize proteins by using several transport mechanisms and the amino acids contents in their cytoplasms (7,8,9). PS (phosphatidylserine) exposure is recognized as a marker of cell death as well as being an activation marker.…”

Section: Introductionmentioning

confidence: 99%

Oxidative alterations during human platelet storage

Göker¹

2011

mpj

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SUMMARY: During storage of platelet obtained by apheresis several changes occur. The aim of this study was to investigate the effect of storage on activation, apoptosis, protein pattern, lipid peroxidation, and the levels of nitric oxide (NO) and glutathione (GSH) of platelets. In this study, platelets obtained from healty donors (n=7) by apheresis were kept in an agitator for nine days at 20-24°C. The samples were taken on the 1st, 3 rd, 5 th and 9 th days and platelets were precipitated. Platelet activation with PAC-1 and CD62-P antibodies and platelet apoptosis were measured with Annexin-V using flow cytometer. Platelets were frozen and thawed four times and then NO, GSH and malondialdehyte (MDA) levels were assayed by spectrophotometry. Platelets protein pattern was investigated via sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) procedure. When compared to the 1st day, platelet CD62-P, PAC-1 expressions and Annexin-V levels significantly increased on the 3rd, 5th and 9th days, while platelet NO and GSH levels significantly decreased on the 3rd, 5th and 9th days. Furthermore MDA levels significantly increased on only the 5th and 9th days. Mild changes occurred in the density of platelet protein bands. In conclusion, our results show that alterations of platelet activity during storage period may enhance platelet procoagulant activity which increases trombogenic risk. Therefore, for transfusion using fresh platelets or adjusting platelet preservation are strongly important for platelet behavior in vivo conditions.

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Section: Introductionmentioning

confidence: 99%

Oxidative alterations during human platelet storage

Göker¹

2011

mpj

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“…Platelets from hypercholesterolemic humans have increased cholesterol content and hypersensitivity to endogenous aggregating agonists [9,21,25]. In familial hypercholesterolemic patients, cholesterol-lowering treatment with statin, an HMG-CoA reductase inhibitor, decreases the platelet cholesterol content and platelet sensitivity to the aggregating agonists such as ADP and collagen [9,17,18].…”

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confidence: 99%

Modulation of Rabbit Platelet Aggregation and Calcium Mobilization by Platelet Cholesterol Content

Shiraishi

Tani

Miyamoto

2010

The Journal of Veterinary Medical Science

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ABSTRACT. Hypercholesterolemia is one of the major contributing factors in atherosclerosis and the development of cardiovascular disease. Platelets from hypercholesterolemic rabbit have an increased cholesterol content and a hypersensitivity to endogenous aggregating agonists. Although rabbit has been widely used in studies of hypercholesterolemia, the precise role of platelet cholesterol in rabbit platelet activation has not been studied. In the present study, to determine the direct role of cholesterol on rabbit platelet activation, we examined the effect of in vitro modulation of cholesterol content on platelet activation. Cholesterol-depleted rabbit platelets by the treatment with methyl--cyclodextrin showed decreased platelet aggregation by physiological agonists such as thrombin, adenosine diphosphate, and collagen. The inhibition of thrombin-induced aggregation in cholesterol-depleted platelets was restored by cholesterol repletion in platelets. The cholesterol depletion also inhibited Ca 2+ mobilization, which plays a pivotal role in the platelet activation induced by physiological agonists. We showed that the Ca 2+ influx pathway is strongly suppressed by cholesterol depletion more than Ca 2+ release from intracellular Ca 2+ stores in platelets stimulated with thrombin. Furthermore, platelet aggregation induced by PMA, a potent protein kinase C activator, was also depressed by cholesterol depletion. On the other hand, cholesterol enrichment in platelets augmented thrombininduced aggregation and Ca 2+ mobilization. These findings suggest that cholesterol plays a critical role in regulating rabbit platelet activation, and provides fundamental information regarding hypercholesterolemia-mediated effects on cells in the rabbit model.

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“…Çekirdekli hücrelerde PS'in hücre zarı dış yüzeyine hareketi tam olarak bir apoptoz belirteci iken trombositlerde apoptozdan ziyade aktivasyonu düşündürmektedir. Trombosit aktivasyonu ve apoptozu benzer özellikler gösterirler (PS translokasyonu, mikropartikül oluşumu gibi) ki bu durum trombosit aktivasyonunun apoptoza ilerlediğini düşündür-mektedir (28,29). Ancak, trombosit apoptozunun ve aktivasyonunun birbirinden farklı ilerleyebileceğini gösteren çalış-malar da mevcuttur (30).…”

Section: Discussionunclassified