A5006091584- Psoriasis: Treatment and Pathogenesis
- Dermatology and Skin Diseases
- Asthma and respiratory diseases
- Atherosclerosis and Cardiovascular Diseases
- Sodium Intake and Health
- Cytokine Signaling Pathways and Interactions
- Nitric Oxide and Endothelin Effects
- Blood Coagulation and Thrombosis Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Venous Thromboembolism Diagnosis and Management
- Immune Response and Inflammation
- Adipokines, Inflammation, and Metabolic Diseases
- Eicosanoids and Hypertension Pharmacology
- Renin-Angiotensin System Studies
- Cardiac Fibrosis and Remodeling
- Neuroinflammation and Neurodegeneration Mechanisms
- Heme Oxygenase-1 and Carbon Monoxide
- Immune cells in cancer
- Antiplatelet Therapy and Cardiovascular Diseases
- Traumatic Brain Injury and Neurovascular Disturbances
- Apelin-related biomedical research
- Cardiovascular Disease and Adiposity
- Vitamin D Research Studies
- IL-33, ST2, and ILC Pathways
- Inflammation biomarkers and pathways
Johannes Gutenberg University Mainz
2016-2025
University Medical Center of the Johannes Gutenberg University Mainz
2016-2025
German Centre for Cardiovascular Research
2018-2024
Klinik und Poliklinik für Psychosomatische Medizin und Psychotherapie
2023
Zero to Three
2023
University of Duisburg-Essen
2020
Emory University
2020
University of Cologne
2020
University Medical Center
2011-2018
Veneto Institute of Molecular Medicine
2016
Angiotensin II (ATII), a potent vasoconstrictor, causes hypertension, promotes infiltration of myelomonocytic cells into the vessel wall, and stimulates both vascular inflammatory cell NADPH oxidases. The predominant source reactive oxygen species, eg, (endothelial, smooth muscle, adventitial) versus phagocytic oxidase, role in mediating arterial hypertension have not been defined yet. (1 mg · kg(-1) d(-1) for 7 days) increased number CD11b(+)Gr-1(low)F4/80(+) macrophages...
Background The gut microbiome is essential for physiological host responses and development of immune functions. impact microbiota on blood pressure systemic vascular function, processes that are determined by cell unknown. Methods Results Unchallenged germ‐free mice ( GF ) had a dampened T helper type 1 skewing compared to conventionally raised CONV ‐R) mice. Colonization with regular induced lymphoid mRNA transcription T‐box expression in cells resulted mild endothelial dysfunction....
Interleukin (IL)-17A is regarded as an important cytokine to drive psoriasis, inflammatory skin disease marked by increased cardiovascular mortality. We aimed test the hypothesis that overproduction of IL-17A in leading dermal inflammation may systemically cause vascular dysfunction psoriasis-like disease.Conditional overexpression keratinocytes caused severe mice (K14-IL-17A(ind/+) mice), associated with reactive oxygen species formation and circulating CD11b(+) leukocytes blood,...
Dipeptidyl peptidase-4 (DPP-4) inhibitors are a novel class of drugs for the treatment hyperglycaemia. Preliminary evidence suggests that their antioxidant and anti-inflammatory effects may have beneficial on cardiovascular complications diabetes. In present study, we investigate in an experimental sepsis model whether linagliptin exerts pleiotropic vascular independent its glucose-lowering properties. Linagliptin (83 mg/kg chow 7days) was administered rat lipopolysaccharide (LPS) (10 mg/kg,...
Immune cells contribute to angiotensin II (ATII)-induced vascular dysfunction and inflammation. Interferon-γ (IFN-γ), an inflammatory cytokine exclusively produced by immune cells, seems be involved in ATII-driven cardiovascular injury, but the actions cellular source of IFN-γ remain incompletely understood.IFN-γ(-/-) Tbx21(-/-) mice were partially protected from ATII-induced (1 mg/kg per day ATII, infused subcutaneously miniosmotic pumps) endothelial smooth muscle dysfunction, whereas...
Skin inflammation inhibits bone formation through IL-17A.
Endothelial nitric-oxide synthase (eNOS) uncoupling and increased inducible NOS (iNOS) activity amplify vascular oxidative stress. The role of inflammatory myelomonocytic cells as mediators these processes their impact on tetrahydrobiopterin availability function have not yet been defined. Angiotensin II (ATII, 1 mg/kg/day for 7 days) Ly6Chigh CD11b+/iNOShigh leukocytes up-regulated levels eNOS glutathionylation in aortas C57BL/6 mice. Vascular iNOS-dependent NO formation was increased,...
Multicellular interactions of platelets, leukocytes, and the blood vessel wall support coagulation precipitate arterial venous thrombosis. High levels angiotensin II cause hypertension by a complex vascular inflammatory pathway that requires leukocyte recruitment reactive oxygen species production is followed dysfunction. We delineate previously undescribed, proinflammatory coagulation-vascular circuit major regulator tone, pressure, endothelial function. In mice with II-induced...
Heme oxygenase-1 (HO-1) confers protection to the vasculature and suppresses inflammatory properties of monocytes macrophages. It is unclear how HO-1 determines extent vascular dysfunction in mice humans. Decreased activity expression was paralleled by increased aortic nicotinamide dinucleotide phosphate oxidase Nox2 deficient Hmox1−/− Hmox1+/− compared with Hmox1+/+ mice. When subjected angiotensin II-infusion, streptozotocin-induced diabetes mellitus aging, showed inversely correlated HO...
Conventional Ly6C hi monocytes have developmental plasticity for a spectrum of differentiated phagocytes. Here we show, using conditional deletion strategies in mouse model Toll-like receptor (TLR) 7-induced inflammation, that the cell fates monocytes, and resultant is coordinately regulated by TLR Notch signaling. Cell-intrinsic Notch2 TLR7-Myd88 pathways independently synergistically promote lo patrolling monocyte development from under inflammatory conditions, while impairment either...
We have reported earlier that a high salt intake triggered an aestivation-like natriuretic-ureotelic body water conservation response lowered muscle mass and increased blood pressure. Here, we tested the hypothesis similar adaptive occurs in experimental chronic renal failure.In four subsequent experiments Sprague Dawley rats, used surgical 5/6 reduction (5/6 Nx) to induce failure. studied solute excretion 24-hour metabolic cage experiments, pressure by radiotelemetry, adjustment liver...
Abstract Aim Recent evidence suggests that arterial hypertension could be alternatively explained as a physiological adaptation response to water shortage, termed aestivation, which relies on complex multi‐organ metabolic adjustments prevent dehydration. Here, we tested the hypothesis chronic loss across diseased skin leads similar adaptive conservation responses observed in experimental renal failure or high salt diet. Methods We studied mice with keratinocyte‐specific overexpression of...
Traffic noise may play an important role in the development and deterioration of ischaemic heart disease. Thus, we sought to determine mechanisms cardiovascular dysfunction inflammation induced by aircraft a mouse model myocardial infarction (MI) humans with incident MI.C57BL/6J mice were exposed alone (average sound pressure level 72 dB; peak 85 dB) for up 4 days, resulting pro-inflammatory aortic gene expression myeloid cell adhesion/diapedesis pathways. The promoted adhesion infiltration...
Abstract Aims Epidemiology links noise to increased risk of metabolic diseases like diabetes and obesity. Translational studies in humans experimental animals showed that causes reactive oxygen species (ROS)–mediated cardiovascular damage. The interaction between diabetes, specifically potential additive adverse effects, remains be determined. Methods results C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/day for 5 days) induce type 1 mellitus, S961 (subcutaneous...
We examined the cardiovascular effects of celiac disease (CeD) in a humanized mouse model, with focus on vascular inflammation, endothelial dysfunction, and oxidative stress. NOD.DQ8 mice genetically predisposed to CeD were subjected diet regime oral gavage induce (gluten group vs. control). tested function, confirmed indicators, evaluated inflammation stress various tissues. Plasma proteome profiling was also performed. markers gluten group, indicating increased blood pressure impaired...
The organic nitrate pentaerythritol tetranitrate is devoid of tolerance, which has been attributed to the induction antioxidant enzyme heme oxygenase (HO)-1. With present study, we tested whether chronic treatment with can improve angiotensin II-induced vascular oxidative stress and dysfunction. In contrast isosorbide-5 mononitrate (75 mg/kg per day for 7 days), (15 days) improved impaired endothelial smooth muscle function normalized cardiac reactive oxygen species production (mitochondria,...
Abstract Aims Heart failure (HF) ensuing myocardial infarction (MI) is characterized by the initiation of a systemic inflammatory response. We aimed to elucidate impact myelomonocytic cells and their activation angiotensin II on vascular endothelial function in mouse model HF after MI. Methods results was induced male C57BL/6J mice permanent ligation left anterior descending coronary artery. Compared sham, had significantly impaired accompanied enhanced mobilization Sca-1+c-Kit+...
Despite major advances in acute interventions for myocardial infarction (MI), adverse cardiac remodeling and excess fibrosis after MI causing ischemic heart failure (IHF) remain a leading cause of death worldwide. Here we identify profibrotic coagulation signaling pathway that can be targeted improved function following with persistent ischemia. Quantitative phosphoproteomics tissue revealed an upregulated mitogen-activated protein kinase (MAPK) human IHF. Intervention this trametinib...
Heart failure (HF) coincides with cardiomyocyte telomere shortening. Arterial hypertension is the most prominent risk factor for HF. Both HF and arterial are associated dysregulation of neurohormonal axis. How activation linked to shortening in pathogenesis incompletely understood. Cardiomyocyte length was assessed a mouse model hypertensive induced by excess (AngII [angiotensin II] infusion, high salt diet, uninephrectomy), AngII-stimulated cardiomyocytes endomyocardial biopsies from...