A5089606483- Protein Tyrosine Phosphatases
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cardiovascular Disease and Adiposity
- Cerebrovascular and genetic disorders
- Extracellular vesicles in disease
- Galectins and Cancer Biology
- Blood Coagulation and Thrombosis Mechanisms
- Macrophage Migration Inhibitory Factor
- Regulation of Appetite and Obesity
- Adipose Tissue and Metabolism
- Systemic Sclerosis and Related Diseases
- Platelet Disorders and Treatments
- Venous Thromboembolism Diagnosis and Management
- Erythrocyte Function and Pathophysiology
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Nitric Oxide and Endothelin Effects
- Adipokines, Inflammation, and Metabolic Diseases
- Inflammation biomarkers and pathways
University Medical Center of the Johannes Gutenberg University Mainz
2021-2024
Johannes Gutenberg University Mainz
2021-2024
Endothelial activation promotes the release of procoagulant extracellular vesicles and inflammatory mediators from specialized storage granules. membrane exocytosis is controlled by phosphorylation. We hypothesized that absence PTP1B (protein tyrosine phosphatase 1B) in endothelial cells venous thromboinflammation triggering fusion exocytosis. Mice with inducible deletion (End.PTP1B-KO) underwent inferior vena cava ligation to induce stenosis thrombosis. Primary transgenic mice human...
The Fourth Maastricht Consensus Conference on Thrombosis included the following themes. Theme 1: "coagulome" as a critical driver of cardiovascular disease. Blood coagulation proteins also play divergent roles in biology and pathophysiology, related to specific organs, including brain, heart, bone marrow, kidney. Four investigators shared their views these organ-specific topics. 2: Novel mechanisms thrombosis. Mechanisms linking factor XII fibrin, structural physical properties, contribute...
Abstract Obesity promotes endothelial dysfunction. Endothelial cells not only respond, but possibly actively promote the development of obesity and metabolic Our aim was to characterize role leptin receptors (LepR) for whole body metabolism diet-induced obesity. Mice with tamoxifen-inducible, Tie2.Cre-ER T2 -mediated deletion LepR in (End.LepR knockout, KO) were fed high-fat diet (HFD) 16 weeks. Body weight gain, serum levels, visceral adiposity adipose tissue inflammation more pronounced...
The cytokine interleukin-6 (IL-6) plays a central role in the inflammation cascade as well cardiovascular disease progression. Since myeloid cells are primary source of IL-6 formation, we aimed to generate mouse model study cell-derived vascular disease.
Erythrocytes (red blood cells) participate in the control of vascular NO bioavailability. The purpose this study was to determine whether and how genetic deletion ARG1 (arginase-1) affects smooth muscle cell signaling, osteoblastic differentiation, atherosclerotic lesion calcification.Atherosclerosis-prone mice with conditional, erythrocyte-restricted (apoE-/- red cell.ARG1 knockout) were generated calcification studied using molecular imaging osteogenic activity agent OsteoSense, Alizarin...
Background Smooth muscle cell (SMC) phenotype switching plays a central role during vascular remodeling. Growth factor receptors are negatively regulated by protein tyrosine phosphatases (PTPs), including its prototype PTP1B. Here, we examine how reduction of PTP1B in SMCs affects the remodeling response to injury. Methods Mice with inducible deletion (SMC.PTP1B-KO) were generated crossing mice expressing Cre.ERT2 recombinase under Myh11 promoter PTP1Bflox/flox and subjected FeCl3 carotid...