A5067661704- Bone Metabolism and Diseases
- Rheumatoid Arthritis Research and Therapies
- Bone health and treatments
- Bone and Joint Diseases
- Cytokine Signaling Pathways and Interactions
- Autoimmune and Inflammatory Disorders Research
- Osteoarthritis Treatment and Mechanisms
- Cell Adhesion Molecules Research
- Systemic Lupus Erythematosus Research
- Spondyloarthritis Studies and Treatments
- NF-κB Signaling Pathways
- MicroRNA in disease regulation
- Immunotherapy and Immune Responses
- Orthopedic Infections and Treatments
- Monoclonal and Polyclonal Antibodies Research
- Biomarkers in Disease Mechanisms
- Viral Infections and Immunology Research
- interferon and immune responses
- Bone health and osteoporosis research
- Reproductive System and Pregnancy
- Medical Imaging Techniques and Applications
- Muscle Physiology and Disorders
- PI3K/AKT/mTOR signaling in cancer
- Mast cells and histamine
- Ion channel regulation and function
Medical University of Vienna
2012-2023
Karl Landsteiner Society
2022
Klinik Hietzing
2022
Center for Rheumatology
2001-2013
Ludwig Boltzmann Cluster for Cardiovascular Research
2012
Palmetto Hematology Oncology
2012
Novartis Institutes for BioMedical Research
2007
Novartis (Switzerland)
2007
University of Vienna
1997-2004
Krankenhaus Bruneck
2004
The detailed cellular and molecular mechanisms leading to joint destruction in rheumatoid arthritis, a disease driven by proinflammatory cytokines, are still unknown. To address the question of whether osteoclasts play pivotal role this process, transgenic mice that express human TNF (hTNFtg) develop severe destructive arthritis were crossed with osteopetrotic, c-fos–deficient (c-fos–/–) completely lacking osteoclasts. resulting mutant (c-fos–/–hTNFtg) developed TNF-dependent absence All...
Osteoprotegerin is a novel member of the tumor necrosis factor receptor superfamily and soluble decoy activator nuclear factor-kappaB ligand. Recent experimental research has implicated osteoprotegerin in atherogenesis, but epidemiological confirmation this concept sparse.As part prospective, population-based Bruneck Study, severity, initiation, progression atherosclerosis were assessed carotid arteries. Cases incident cardiovascular disease vascular mortality carefully recorded over 10-year...
The detailed cellular and molecular mechanisms leading to joint destruction in rheumatoid arthritis, a disease driven by proinflammatory cytokines, are still unknown. To address the question of whether osteoclasts play pivotal role this process, transgenic mice that express human TNF (hTNFtg) develop severe destructive arthritis were crossed with osteopetrotic, c-fos–deficient (c-fos–/–) completely lacking osteoclasts. resulting mutant (c-fos–/–hTNFtg) developed TNF-dependent absence All...
MicroRNAs (miRNA) are a new class of regulatory elements. Altered expression miRNA has been demonstrated in the inflamed joints patients with rheumatoid arthritis (RA). The aim this study was to examine role pathogenesis autoimmune arthritis, using 2 murine models.Collagen-induced (CIA) and K/BxN serum-transfer were induced wild-type (WT) miR-155-deficient (miR-155(-/-) ) mice. severity determined clinically histologically. Anticollagen antibodies cytokines measured by enzyme-linked...
To investigate whether stress- and mitogen-activated protein kinases (SAPK/MAPK), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal (JNK), p38 MAPK, are significantly activated in rheumatoid arthritis (RA) synovial tissue compared with their activation degenerative joint disease; to assess the localization of SAPK/MAPK tissue; search for factors leading stress human cells.Immunoblotting immunohistology by antibodies specific forms were performed on samples from patients...
To investigate the efficacy of single and combined blockade tumor necrosis factor (TNF), interleukin-1 (IL-1), RANKL pathways on synovial inflammation, bone erosion, cartilage destruction in a TNF-driven arthritis model.Human TNF-transgenic (hTNFtg) mice were treated with anti-TNF (infliximab), IL-1 receptor antagonist (IL-1Ra; anakinra), or osteoprotegerin (OPG; an OPG-Fc fusion protein), either alone combinations 2 agents all 3 agents. Synovial damage evaluated histologically.Synovial...
Abstract Objective To study the effects of osteoclast‐targeted therapies, such as osteoprotegerin (OPG) and pamidronate, on joint inflammation bone destruction using a tumor necrosis factor α (TNFα)‐transgenic mouse model. Methods Mice were placed into 5 groups that received either OPG, combination both agents, infliximab positive control, or phosphate buffered saline negative control. Treatment was initiated at onset arthritis, continued over 6 weeks, thereafter, clinical, radiologic,...
Blocking TNF effectively inhibits inflammation and structural damage in human rheumatoid arthritis (RA). However, so far it is unclear whether the effect of a direct one or indirect on up-regulation other mediators. IL-1 may be these candidates because has central role animal models arthritis, inhibition used as therapy RA. We removed effects from TNF-mediated inflammatory joint disease by crossing IL-1alpha beta-deficient mice (IL-1-/-) with arthritic TNF-transgenic (hTNFtg) mice....
Heat shock proteins (hsp) have been repeatedly implicated to participate in the pathogenesis of rheumatoid arthritis (RA). Herein, we investigated regulation synovial hsp70 expression by analyzing DNA-binding activity heat transcription factor 1 (HSF1) as well inducible expression. Experiments were performed both on tissue and fibroblast-like cells (SFC). Gel mobility shift analysis revealed increased HSF1 activation, Western blotting immunohistochemistry RA tissue, but not derived from...
Objectives: Chronic inflammation is a major risk factor for systemic bone loss leading to osteoporotic fracture and substantial morbidity mortality. Inflammatory cytokines, particularly tumour necrosis (TNF) interleukin-1 (IL1), are thought play key role in the pathogenesis of inflammation-induced loss, but their exact roles yet be determined. Methods: To determine whether TNF directly triggers or requires IL1, human TNFα mice (hTNFtg) were crossed with lacking IL1α IL1β (IL1 −/− hTNFtg)....
Abstract Objective To determine the effect of joint protection and home exercises on hand function patients with osteoarthritis (OA). Methods Randomized, controlled, 3‐month trial a blinded assessor. Primary outcome parameter was grip strength; secondary parameters were Health Assessment Questionnaire visual analog scales (VAS) for pain global function. Forty OA randomly assigned to 2 groups: One group received instruction (JPE group), control an information session about OA. Results Grip...
Abstract Objective To investigate the role of tumor necrosis factor (TNF) in systemic bone loss chronic inflammatory conditions, such as rheumatoid arthritis (RA), and to address therapeutic potential osteoclast blockade. Methods We investigated changes human TNF transgenic (hTNFtg) mice, which spontaneously developed severe arthritis. Results Osteodensitometry revealed a significant decrease trabecular mineral density (BMD) (−37%) hTNFtg histomorphometry dramatic volume (−85%) compared with...
Abstract Rheumatoid arthritis (RA) leads to destruction of cartilage and bone. Whether rheumatoid also affects the adjacent bone marrow is less clear. In this study, we investigated subcortical changes in joints from patients with RA. We describe penetration cortical barrier by synovial inflammatory tissue, invasion into cavity formation mononuclear cell aggregates B cells as predominant phenotype. expressed common markers, such CD20, CD45RA, CD79a, were mature cells, indicated CD27...
Abstract Objective To investigate whether activation of p38 MAPK is a crucial signaling factor in inflammatory bone destruction mediated by tumor necrosis (TNF). Mice overexpressing TNF were treated with 2 different inhibitors MAPK, and the effect this treatment on joint inflammation structural damage was assessed. Methods Human TNF‐transgenic mice received systemic (RO4399247 AVE8677). Treatment started at time symptom onset lasted for 6 weeks. assessed clinical signs arthritis, erosion,...
Heme oxygenase 1 (HO-1) plays an important role in vascular disease, transplantation, and inflammation. In animal models of acute chronic inflammation, induction HO-1 has anti-inflammatory cytoprotective properties. Since inflammation is trigger osteoclastogenesis, we hypothesized that might influence osteoclastogenesis. We investigated the effects on osteoclast formation vitro vivo. Furthermore, addressed inflammatory bone loss humans. When was induced by hemin vitro, a significant...
<h3>Objective</h3> To elucidate the mechanisms involved in cartilage damage an experimental model of rheumatoid arthritis (RA) by specifically addressing time course extracellular matrix degradation and contribution cell–matrix interactions for initiation perpetuation this process. <h3>Methods</h3> The human tumour necrosis factor (TNF) transgenic (hTNFtg) mouse RA was used to analyse pannus attachment destruction, respectively, crossed hTNFtg mice with interleukin (IL)-1<sup>−/−</sup>...