Lipid peroxidation by activated platelets: A possible link between thrombosis and atherogenesis

Görög, P.; Kovács, Iren B.

doi:10.1016/0021-9150(94)05506-e

Cited by 31 publications

(15 citation statements)

References 17 publications

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“…In particular, leptin appears to represent a novel, direct link between obesity and cardiovascular disease [10,24,25], and studies in the mouse suggest that platelets may be a critical component of this link [11,12]. As platelet activation plays a key role in the formation of arterial thrombi [26] and in many of the inflammatory processes that accompany the development of atherosclerotic plaques [27,28], we sought to determine the influence of leptin on human platelet function. We thus examined the effect of leptin on the activation of platelets from 56 different donors.…”

Section: Discussionmentioning

confidence: 99%

The leptin receptor system of human platelets

Dellas

et al. 2005

Journal of Thrombosis and Haemostasis

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Summary. Obesity is associated with elevated levels of leptin in the blood. Elevated leptin is a risk factor for thrombosis in humans, and leptin administration promotes platelet activation and thrombosis in the mouse. The current study examines the effect of leptin on human platelets, and provides initial insights into the nature of the leptin receptor on these platelets. Leptin potentiated the aggregation of human platelets induced by low concentrations of ADP, collagen and epinephrine. However, the response varied significantly between donors, with platelets from some donors (approximately 40%) consistently responding to leptin (responders) and those from other donors (approximately 60%) never responding (non-responders). Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) experiments showed that platelets from both groups only express the signaling form of the leptin receptor, and that responder platelets express higher levels of this receptor than nonresponders. Ligand-binding assays demonstrate specific, saturable binding of leptin to platelets from both groups with apparent K d values of 76 ± 20 nM for responders and 158 ± 46 nM for non-responders. Thus, the decreased sensitivity of non-responder platelets to leptin does not result from the absence of the signaling form of this receptor, but may reflect differences in its level of expression and/or affinity for leptin. These preliminary studies demonstrate that platelets are a major source of leptin receptor in the circulation, and suggest that leptin-responsive individuals may have a higher risk for obesity-associated thrombosis than non-responsive individuals.

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Section: Discussionmentioning

confidence: 99%

The leptin receptor system of human platelets

Dellas

et al. 2005

Journal of Thrombosis and Haemostasis

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“…Atherosclerosis is the major cause of CVD, and a key event in this inflammatory process is accumulation of lipoproteins within the arterial wall . Modified low‐density lipoprotein (LDL) exerts various effects supporting atherogenesis, including increased expression of adhesion molecules, leukocyte adhesion and chemotaxis, injury to endothelial cells, enhanced foam cell formation, increased smooth muscle cell and fibroblast proliferation and release of inflammatory mediators …”

Section: Introductionmentioning

confidence: 99%

Lipoprotein modifications by gingipains of Porphyromonas gingivalis

Lönn

Ljunggren

Klarström-Engström

et al. 2018

J of Periodontal Research

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Background and ObjectiveSeveral studies have shown an association between periodontitis and cardiovascular disease (CVD). Atherosclerosis is the major cause of CVD, and a key event in the development of atherosclerosis is accumulation of lipoproteins within the arterial wall. Bacteria are the primary etiologic agents in periodontitis and Porphyromonas gingivalis is the major pathogen in the disease. Several studies support a role of modified low‐density lipoprotein (LDL) in atherogenesis; however, the pathogenic stimuli that induce the changes and the mechanisms by which this occur are unknown. This study aims to identify alterations in plasma lipoproteins induced by the periodontopathic species of bacterium, P. gingivalis, in vitro.Material and MethodsPlasma lipoproteins were isolated from whole blood treated with wild‐type and gingipain‐mutant (lacking either the Rgp‐ or Kgp gingipains) P. gingivalis by density/gradient‐ultracentrifugation and were studied using 2‐dimensional gel electrophoresis followed by matrix‐assisted laser desorption/ionization mass spectrometry. Porphyromonas gingivalis‐induced lipid peroxidation and antioxidant levels were measured by thiobarbituric acid‐reactive substances and antioxidant assay kits, respectively, and lumiaggregometry was used for measurement of reactive oxygen species (ROS) and aggregation.Results Porphyromonas gingivalis exerted substantial proteolytic effects on the lipoproteins. The Rgp gingipains were responsible for producing 2 apoE fragments, as well as 2 apoB‐100 fragments, in LDL, and the Kgp gingipain produced an unidentified fragment in high‐density lipoproteins. Porphyromonas gingivalis and its different gingipain variants induced ROS and consumed antioxidants. Both the Rgp and Kgp gingipains were involved in inducing lipid peroxidation.Conclusion Porphyromonas gingivalis has the potential to change the expression of lipoproteins in blood, which may represent a crucial link between periodontitis and CVD.

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“…Lipid peroxidation severely damages the cell membrane and compromises cell function, mainly by damaging the vascular endothelium cells, causing vasoconstriction (Katusic et al, 1993), thrombosis (Gorog and Kovacs, 1995) and vascular remodelling (Xiang et al, 2002;Wedgwood and Black, 2003;Matsui et al, 2004), which then lead to an increase in pulmonary artery resistance and pulmonary hypertension.…”

Section: Introductionmentioning

confidence: 99%

Effects of early feed restriction and cold temperature on lipid peroxidation, pulmonary vascular remodelling and ascites morbidity in broilers under normal and cold temperature

Pan

Tan²,

Li³

et al. 2005

British Poultry Science

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Two experiments were conducted to evaluate the effects of early feed restriction on lipid peroxidation, pulmonary vascular remodelling and ascites incidence in broilers under normal and low ambient temperature. In experiment 1, the restricted birds were fed 8h per day either from 7 to 14 d or from 7 to 21 d, while the controlled birds were fed ad libitum. In experiment 2, the restricted birds were fed 80 or 60% of the previous 24-h feed consumption of full-fed controls for 7 d from 7 to 14 d. On d 14, half of the birds in each treatment both in experiment 1 and experiment 2 were exposed to low ambient temperature to induce ascites. Body weight and feed conversion ratio were measured weekly. The incidences of ascites and other disease were recorded to determine ascites morbidity and total mortality. Blood samples were taken on d 14, 21, 28, 35 and 42 to measure the plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). On d 42, samples were taken to determine the right/total ventricular weight ratio (RV/TV), vessel wall area/vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA). Low-temperature treatment increased plasma MDA concentration. When broilers were exposed to a cool environment for 3 weeks, plasma SOD and GSH-Px activity were decreased compared with normal-temperature chicks. RV/TV, WA/TA and mMTPA on d 42 were increased in birds exposed to cold, consistent with the increased pulmonary hypertension and ascites morbidity. Early feed restriction markedly decreased plasma MDA concentration. The plasma SOD and GSH-Px activity of feed-restricted birds were markedly higher than those fed ad libitum on d 35 and d 42. All early feed restriction treatments reduced ascites morbidity and total mortality. On d 42, the RV/TV, WA/TA and mMTPA of feed-restricted broilers were lower than that of the ad libitum-fed broilers. The results suggested that early feed restriction alleviated the lipid peroxidation, promoted the activity of enzymatic antioxidant and inhibited pulmonary vascular remodelling. These changes might be associated with reduced ascites incidence.

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Lipid peroxidation by activated platelets: A possible link between thrombosis and atherogenesis

Cited by 31 publications

References 17 publications

The leptin receptor system of human platelets

The leptin receptor system of human platelets

Lipoprotein modifications by gingipains of Porphyromonas gingivalis

Effects of early feed restriction and cold temperature on lipid peroxidation, pulmonary vascular remodelling and ascites morbidity in broilers under normal and cold temperature

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