Influence of low density lipoproteins on cytosolic free Ca2+ concentration and dense tubular system in human platelets

Zhao, Bin; Dierichs, R.; Liu, J.F.; Zhu, Zhiming; Berkes, P.; Frye, S.

doi:10.1016/0049-3848(93)90170-s

Cited by 13 publications

(4 citation statements)

References 17 publications

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“…Furthermore, the open canalicular system at the activation stage is able to increase the platelet surface by evagination [32]. One of our earlier papers has shown that native LDL induces functional morphological change by means of promoting the calcium influx [28]. The effect caused by we excluded an influence of dilution and temperature.…”

Section: Discussionmentioning

confidence: 85%

“…It has been reported that platelet adhesiveness to glass could be enhanced by aggregating agents and probably by plasma protein as well [26,27]. Since native and oxidized LDL induce alterations on platelet morphology and provoke platelet activation, they are regarded to be platelet agonists [7,8,9,28]. As platelets are stimulated, the first physiological responses are platelet adhesion and shape change accompanied by degranulation.…”

Section: Discussionmentioning

confidence: 99%

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Adhesion of washed blood platelets in vitro is advanced, accelerated, and enlarged by oxidized low‐density lipoprotein

Zhao

Rickert

Filler³

et al. 1995

American J Hematol

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In order to study the influence of oxidized low-density lipoprotein (Ox-LDL) on platelet functional morphology at an early activation stage, washed human blood platelets were stimulated by 100 micrograms/ml Ox-LDL at 37 degrees C. The settling and spreading process of stimulated and unstimulated platelets on Formvar-coated glass was observed for approximately 20 min by reflection contrast microscopy (RCM) and quantified by image analysis. Each group consisted of at least 250 platelets. The results show that incubation with Ox-LDL causes platelet shape change and pseudopodia formation. The sedimentation of stimulated platelets precedes that of unstimulated platelets by approximately 3 min. The increase of the total adhesion area of all Ox-LDL treated platelets is significantly accelerated in comparison to normal platelets (20.45 microns2/min vs. 15.45 microns2/min; P < 0.01). The mean total adhesion area of Ox-LDL-treated platelets was generally larger than that of untreated platelets (189.7 microns2 vs. 144.7 microns2; P < 0.01). The disappearance of intracellular granules after platelet activation, observed by RCM, is supported by transmission electron microscopy. Our results suggest that Ox-LDL activates platelets and advances and accelerates their adhesion and thereby may contribute to pathological thrombosis and arteriosclerosis.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Adhesion of washed blood platelets in vitro is advanced, accelerated, and enlarged by oxidized low‐density lipoprotein

Zhao

Rickert

Filler³

et al. 1995

American J Hematol

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“…The latter represents an invagination of the plasma membrane providing a connection with the outer milieu via pores at the surface and a two-way channel for uptake of particles and the delivery of granular contents during activation and degranulation [24,34,35,[63][64][65]. Furthermore, the dense tubular system (DTS), originating from the endoplasmic reticulum of MKs [66][67][68][69][70][71][72][73][74][75][76] and small Golgi systems [47,[77][78][79][80], has been described. Three types of PLT granules have been identified morphologically and by histochemical and immunohistochemical methods: dense granules [22,80], α-granules [28,30,58,[82][83][84][85], and lysosomes [72,78].…”

Section: Historical Overviewmentioning

confidence: 99%

Transmission Electron Microscopy of Platelets FROM Apheresis and Buffy-Coat-Derived Platelet Concentrates

Neumüller¹,

Ellinger²

2015

The Transmission Electron Microscope - Theory and Applications

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Platelet concentrates are produced in order to treat bleeding disorders. They can be provided by apheresis machines or by pooling of buffy coats from four blood donations. During their manufacturing and storage, morphological alterations of platelets occur which can be demonstrated by transmission electron microscopy. Alterations range from slight and reversible changes, such as formation of small cell protrusions and swelling of the surface-connected open canalicular system, to severe structural changes, where platelets undergo transitions from discoid to ameboid shapes as a consequence of platelet activation. These alterations end in delivery of the contents of platelet granules as well as platelet involution caused by apoptosis and necrosis processes denoted as the platelet release reaction. Hereby, the involvement of the network of the open canalicular system, helping to deliver the contents of platelet granules into the surrounding milieu via pores, is distinctly shown by electron tomography. As a consequence of platelet activation, a delivery of differently sized microparticles takes place which is thought to play an important role in the adverse reactions in some recipients of platelet concentrates. In this article, the formation and delivery of platelet microparticles is illustrated by electron tomography. Above all, the ultrastructural features of platelets and megakaryocytes are discussed in the context of the molecular characteristics of the plasma membrane and organelles including the different granules and the expression of receptors engaged in signaling during platelet activation. Starting from the knowledge of the ultrastructure of resting and activated platelets, a score classification is presented, allowing the evaluation of different activation stages in a reproducible manner. Examples of evaluations of platelet concentrates using electron microscopy are briefly reviewed. In the last part,

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“…Low-density lipoproteins (LDL) have been reported to possess platelet activating activities such as the enhancement of platelet sensitivity to stimuli (1)(2)(3)(4) and the induction of platelet aggregation (5)(6). Oxidative modification dramatically changes the biological properties of LDL, converting them into a form that is both atherogenic and pro-thrombotic (7)(8).…”

Section: Introductionmentioning

confidence: 99%

Interaction of LDL and platelets in ischaemic and ischaemic risk subjects

Gupta

Mallika

Srivastava

2005

Indian J Clin Biochem

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Platelets play a vital role in the progression of atherosclerosis and thrombosis, a major cause of death worldwide. Platelets are activated by many triggers like elevated LDL in blood resulting in aggregation and formation of plaque. The purpose of this study was to investigate the effect of LDL and signal transduction inhibitor on the activation of platelets in Ischaemic risk subjects.Platelets from IHD and hyperlipidemic subjects were hypersensitive to ADP, as higher levels of platelet aggregation were observed in these groups. LDL from IHD hypedipidemic subjects was more effective in activating platelets from any other group. Ox-LDL was more effective in activating platelets than native-LDL as monitored by level of platelet aggregation induced by PAF and thrombin. Calcium channel blocker, nifedipine and verapamil inhibited platelet aggregation at micromolar level. Protein kinase inhibitor, staurosporine was effective in inhibiting ADP induced aggregation at nanomolar level.

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Influence of low density lipoproteins on cytosolic free Ca2+ concentration and dense tubular system in human platelets

Cited by 13 publications

References 17 publications

Adhesion of washed blood platelets in vitro is advanced, accelerated, and enlarged by oxidized low‐density lipoprotein

Adhesion of washed blood platelets in vitro is advanced, accelerated, and enlarged by oxidized low‐density lipoprotein

Transmission Electron Microscopy of Platelets FROM Apheresis and Buffy-Coat-Derived Platelet Concentrates

Interaction of LDL and platelets in ischaemic and ischaemic risk subjects

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