Inhibition of Inflammation and Bone Erosion by RNA Interference-Mediated Silencing of Heterogeneous Nuclear RNP A2/B1 in Two Experimental Models of Rheumatoid Arthritis.

Objective: The nuclear protein heterogeneous nuclear RNP A2/B1 (hnRNP A2/B1) is involved in posttranscriptional regulation of gene expression. It is constitutively expressed in lymphoid organs and highly up-regulated in the synovial tissue of patients with rheumatoid arthritis (RA), who may also generate autoantibodies to this protein. This study was undertaken to investigate the potential involvement of hnRNP A2/B1 in the pathogenesis of autoimmune arthritis, by silencing hnRNP A2/B1 expression in 2 animal models of RA.

Cell death and cytokine production induced by autoimmunogenic hydrocarbon oils.

Hydrocarbon oils such as pristane or hexadecane induce arthritis and lupus in rodents sharing clinical and pathological features with the human diseases rheumatoid arthritis and systemic lupus erythematosus, respectively. In pristane-induced lupus in the mouse induction of apoptosis and augmentation of type-I Interferon signalling by pristane have been suggested to contribute to pathology, whereas in pristane-induced arthritis (PIA) in the rat the pathological mechanisms are still elusive. Here we show that pristane induces cell death in rat and human cells.

Regulatory T cells form stable and long-lasting cell cluster with myeloid dendritic cells (DC).

Regulatory T cells (Treg) with the capacity to suppress T-cell proliferation exert various effects on T cell function. In addition, Treg have been shown to modulate the phenotype and function of antigen-presenting cells (APC) including dendritic cells (DC), B cells and monocytes/macrophages. However, the specific mechanism(s) of how Treg affect APC have not been entirely identified so far.

Nucleic acid-stimulated antigen-presenting cells trigger T cells to induce disease in a rat transfer model of inflammatory arthritis.

Autoimmune responses to heterogeneous nuclear ribonucleproteins (hnRNP) occur in many systemic autoimmune diseases, particularly in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus. In RA, humoral and/or cellular autoimmunity to hnRNP-A2/B1 is the most prominent anti-nuclear reactivity, being detectable in more than 50% of patients. However, its pathogenic role has not been fully elucidated yet.

Induction of osteoclast-associated receptor, a key osteoclast costimulation molecule, in rheumatoid arthritis.

Objective: Osteoclast-associated receptor (OSCAR) is a newly identified osteoclast-specific receptor and is of key importance in the process of osteoclast costimulation. This study was undertaken to define the role of costimulation in osteoclast differentiation during inflammatory arthritis.

Methods: OSCAR expression was assessed in the synovium and peripheral blood monocytes of patients with rheumatoid arthritis (RA), and associations with disease activity were assessed.

Four-week dynamic stretching warm-up intervention elicits longer-term performance benefits.

The purpose of this study was to determine whether a dynamic-stretching warm-up (DWU) intervention performed daily over 4 weeks positively influenced power, speed, agility, endurance, flexibility, and strength performance measures in collegiate wrestlers when compared to a static-stretching warm-up (SWU) intervention. Twenty-four male National Collegiate Athletic Association Division I wrestlers were randomly assigned to complete either a 4-week treatment condition (DWU) (n = 11) or an active control condition (SWU) (n = 13) prior to their daily preseason practices. Anthropometric and performance measures were conducted before and after the 4-week experimental period (i.

Molecular mechanisms of inflammatory bone damage: emerging targets for therapy.

Chronic inflammatory bone diseases, such as rheumatoid arthritis (RA), ankylosing spondylitis and periodontal disease, demonstrate the major impact of chronic inflammation on both bone metabolism and bone architecture. During the past decade, scientists have gained increasing insight into the link between inflammation and bone. As a result of new discoveries about the molecular mechanisms of inflammatory bone loss, several molecules have been identified that are attractive and novel targets for the treatment of inflammatory bone loss.