A5015728629- Platelet Disorders and Treatments
- Antiplatelet Therapy and Cardiovascular Diseases
- Inflammatory mediators and NSAID effects
- Eicosanoids and Hypertension Pharmacology
- Sphingolipid Metabolism and Signaling
- Blood properties and coagulation
- Cell Adhesion Molecules Research
- Hormonal and reproductive studies
- Nitric Oxide and Endothelin Effects
- Protein Kinase Regulation and GTPase Signaling
- Pharmacology and Obesity Treatment
- Venous Thromboembolism Diagnosis and Management
- Fatty Acid Research and Health
- Blood Coagulation and Thrombosis Mechanisms
- Cholesterol and Lipid Metabolism
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Peroxisome Proliferator-Activated Receptors
- Hormonal Regulation and Hypertension
- Atherosclerosis and Cardiovascular Diseases
- Blood disorders and treatments
- Receptor Mechanisms and Signaling
- Cellular Mechanics and Interactions
- Atrial Fibrillation Management and Outcomes
- Antioxidant Activity and Oxidative Stress
- Autoimmune Bullous Skin Diseases
Ludwig-Maximilians-Universität München
2011-2022
German Centre for Cardiovascular Research
2015-2022
Institute for Sports Medicine
2005-2021
RWTH Aachen University
2016
University of Amsterdam
2016
Washington University in St. Louis
2016
Maastricht University
2016
Bavarian Research Alliance
2013
LMU Klinikum
2012
Max Planck Institute of Molecular Physiology
2005-2007
Summary Several methods are used to analyse platelet function in whole blood. A new device measure blood aggregation has been developed, called multiple electrode aggregometry (MEA). Our aim was evaluate MEA comparison with the single counting (SPC) method for measurement of and inhibition by aspirin or apyrase diluted Platelet induced different concentrations ADP, collagen TRAP-6 were determined citrateor hirudin-anticoagulated SPC. indicated that spontaneous lower, stimulated higher...
Oxidized low density lipoprotein (LDL) is a key factor in the pathogenesis of atherosclerosis and its thrombotic complications, such as stroke myocardial infarction. It activates endothelial cells platelets through mechanisms that are largely unknown. Here, we show lysophosphatidic acid (LPA) was formed during mild oxidation LDL active compound mildly oxidized minimally modified LDL, initiating platelet activation stimulating cell stress-fiber gap formation. Antagonists LPA receptor...
Atherosclerotic vascular lesions are considered to be a major cause of ischemic diseases, including myocardial infarction and stroke. Platelet adhesion aggregation during ischemia–reperfusion thought the initial steps leading remodeling reocclusion postischemic vasculature. Nitric oxide (NO) inhibits platelet smooth muscle proliferation. A downstream target NO is cyclic guanosine 3′,5′-monophosphate kinase I (cGKI). To test intravascular significance NO/cGKI signaling pathway in vivo, we...
Exogenous unlabeled arachidonic acid (AA) added to human platelets prelabeled with [3H]AA induces breakdown of [3H]phosphatidylinositol and the rapid transient formation [3H]1,2-diacylglycerol [3H] phosphatidic (PA), indicating activation phosphatidylinositol-specific phospholipase C. Formation [3H]PA is inhibited by pretreatment aspirin, which suggests that endoperoxides or thromboxane Az are responsible for AA-induced stimulation AA also [3"P] P A [14C]PA in have been 32PI [14C]AA,...
Lysophosphatidic acid (LPA) is a ligand for LPA(1-3) of the endothelial differentiation gene family G-protein-coupled receptors, and LPA(4-8) related to purinergic receptor. Because structure-activity relationship (SAR) GPR92/LPA(5) limited whether LPA its preferred endogenous has been questioned in literature, this study we applied combination computational experimental site-directed mutagenesis LPA(5) residues predicted interact with headgroup LPA. Four involved recognition were identified...
To study the possible role of catecholamines in platelet activation, aggregation stimulated by ADP, collagen, arachidonic acid and L-epinephrine, thromboxane B2 (TXB2) formation plasma levels renin were studied healthy men both before after 6 days propranolol treatment (40 mg three times daily) under control conditions during sympathoadrenergic stimulation physical exercise (200 W) or smoking. Exercise markedly increased norepinephrine from 128 +/- 28 to 998 418 pg/ml (+/- SD), activity 1.0...
Lipid-rich atherosclerotic plaques are vulnerable, and their rupture can cause the formation of a platelet- fibrin-rich thrombus leading to myocardial infarction ischemic stroke. Although role plaque-based tissue factor as stimulator blood coagulation has been recognized, it is not known whether through direct activation platelets. We isolated lipid-rich atheromatous from 60 patients with carotid stenosis identified morphologically diverse collagen type I- III-positive structures in that...
Lysophosphatidic acid (LPA) is a platelet-activating component of mildly oxidized LDL (mox-LDL) and lipids isolated from human atherosclerotic plaques. Specific antagonists platelet LPA receptors could be useful inhibitors thrombus formation in patients with cardiovascular disease.Short-chain analogs phosphatidic (PA) were examined for their effect on two initial responses, shape change Ca2+ mobilization. Dioctylglycerol pyrophosphate [DGPP(8:0)] dioctylphosphatidic [PA(8:0)], recently...
eicosatetraenoic acid; Hepes, 4-(2-hydroxyethyl)
Human platelets prelabeled with (32P)orthophosphate or [14C]arachidonic acid (AA) were stimulated collagen thrombin, and platelet activation (shape change, aggregation, release of serotonin) was determined in parallel to the formation 32P- 14C-labeled phosphatidic (PA). The results show a close correlation between degree amount PA formed. Activation induced by (2 20 micrograms/ml) blocked pretreatment trifluoperazine, indomethacin, aspirin, N-methylimidazole. This suggests that AA...
We studied the role of tyrosine phosphorylation in induction vascular cell adhesion molecule 1 (VCAM-1), endothelial leukocyte (ELAM-1), and intercellular (ICAM-1) HUVEC. Induction VCAM-1 ELAM-1 surface expression by TNF was dose-dependently reduced pretreatment with protein kinase inhibitors herbimycin A (HMA, IC50 300 nM) or genistein (IC50 30 microM). Only attenuated ICAM-1 induction. Genistein HMA did not affect up-regulation PMA. U937 monocyte to TNF-stimulated HUVEC markedly inhibited...
Abstract Native LDL and oxidized under various conditions were compared in terms of their ability to activate platelets. did not induce platelet shape change or aggregation, even at high concentrations (2 mg protein/mL). was mildly with either CuSO 4 (mox-LDL) 3-( N -morpholino)sydnonimine (SIN-1–LDL). Analysis mox-LDL SIN-1–LDL showed a small increase dienes (E 234nm from 0.28±0.04 0.55±0.09, mean±SD) thiobarbituric acid–reactive substance (from 0 10.6±1.5 nmol/mg, mean±SEM), no apo B...
During long-term dietary n-3 fatty acid supplementation, eicosapentaenoic (EPA) is not incorporated into phosphatidylinositol or -serine of human platelets in vivo and detectable phosphatidic upon stimulation with thrombin.However, EPA released from platelet phospholipids metabolized to thromboxane B3 (TXB,).In contrast, vitro, incorporate [ "CIEPA phosphatidylinositol, whether they contain endogenous their cellular lipids not.Following stimulation, ''CIEPA appears acid, as free transformed...
The influence of reticulated platelets (RPs) on platelet inhibition by ticagrelor when compared with prasugrel is unknown. We aimed to determine the RPs adenosine diphosphate- (ADP-) induced aggregation in patients acute coronary syndrome who were randomly assigned receive either or for P2Y12 receptor inhibition. One hundred and twenty-four prospectively enrolled. immature fraction (IPF) was measured an automated haematoanalyzer assessed multiple electrode aggregometry. In a subgroup (n =...