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Musculo-skeletal joint inflammatory diseases - New vistas from animal model studies – An overview
Ramalingam K*,Mathiyalagan A,Subramanian S,Bharathi Rajan UD
Journal of Biochemical Technology , 2009,
Abstract: The term ‘Arthritis’ refers to all categories of musculo-skeletal joint inflammatory diseases. The different profiles of arthriticmanifestations include rheumatoid arthritis, ankylosing spondylitis,osteoarthritis, polyarthritis, systemic lupus erythematosus (SLE),juvenile arthritis, gout and psoriatic arthritis etc. All theseinflammatory diseases are characterized by chronicity and nonreversible nature of the pathogenesis. All types of arthritis showsome common pathological changes like synovial hypertrophy,microvascular abnormalities, leucocytes infiltration, neovascularisation etc. Though animal model studies on human diseasesmay not fully mimic the real in vivo intricacies of human diseases,certain aspects of such studies and comparison of the findings to real situations may provide insights into the etiological, pathological and therapeutic profiles.
Critical Involvement of Cytokines and Chemokines in the Pathogenesis of Rheumatoid Vasculitis
Tsuyoshi Kasama, Takeo Isozaki, Kuninobu Wakabayashi, Tsuyoshi Odai and Mizuho Matsunawa
Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders , 2012,
Abstract: Vasculitis in rheumatoid arthritis (rheumatoid vasculitis) has a heterogeneous clinical presentation that includes skin disorders, neuropathy, eye symptoms and systemic inflammation. The molecular mechanisms underlying rheumatoid vasculitis are not fully understood; however, the importance of a chronic imbalance of the cytokines and chemokines involved in orchestrating infl ammatory responses is well established in patients with rheumatoid arthritis, and similar dysregulation of these mediators has been suggested to occur in patients with rheumatoid vasculitis. In the present review, we discuss the involvement of cytokines and chemokines in the pathogenesis of rheumatoid vasculitis and evaluate their utility as laboratory parameters of active vasculitic disease. Also the involvement of adhesion molecules is discussed.
Critical Involvement of Cytokines and Chemokines in the Pathogenesis of Rheumatoid Vasculitis
Tsuyoshi Kasama,Takeo Isozaki,Kuninobu Wakabayashi,Tsuyoshi Odai and Mizuho Matsunawa
Clinical Medicine : Arthritis and Musculoskeletal Disorders , 2008,
Abstract: Vasculitis in rheumatoid arthritis (rheumatoid vasculitis) has a heterogeneous clinical presentation that includes skin disorders, neuropathy, eye symptoms and systemic inflammation. The molecular mechanisms underlying rheumatoid vasculitis are not fully understood; however, the importance of a chronic imbalance of the cytokines and chemokines involved in orchestrating infl ammatory responses is well established in patients with rheumatoid arthritis, and similar dysregulation of these mediators has been suggested to occur in patients with rheumatoid vasculitis. In the present review, we discuss the involvement of cytokines and chemokines in the pathogenesis of rheumatoid vasculitis and evaluate their utility as laboratory parameters of active vasculitic disease. Also the involvement of adhesion molecules is discussed.
Cartilage oligomeric matrix protein is involved in human limb development and in the pathogenesis of osteoarthritis
Sebastian Koelling, Till Clauditz, Matthias Kaste, Nicolai Miosge
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar1922
Abstract: Cartilage oligomeric protein (COMP) is a protein of the extracellular matrix and can be found in human articular cartilage [1], meniscus [2], and cruciate ligament and tendon [3]. Lower concentrations of COMP can also be detected in hyaline cartilage of the human rib and trachea [4]. It has also been extracted from animal skeletal tissues, such as bovine tendon and mouse, rat, and porcine cartilage [5]. COMP is an anionic, approximately 550-kDa disulfide-linked pentameric glycoprotein and, as a member of the thrombospondin gene family, is also called thrombospondin 5 [6]. Epidermal growth factor-like and calcium-binding repeats are located in the central region of the protein [7]. The function of COMP is still not completely understood, but it binds to chondrocytes in vitro [8]. COMP has been shown to bind to matrilins [9] and collagen types I, II, and IX [10,11]. In contrast, COMP has no affinity to the other members of the thrombospondin family [12]. The DNA-binding protein SP1 regulates COMP expression [13] and also mechanical compression of chondrocytes [14]. COMP expression has been shown to be inhibited by leukemia/lymphoma-related factor (LRF) [15]. The human COMP gene is located on chromosome 19 [7]. Mutations of this gene can cause pseudoachondroplasia and multiple epiphysial dysplasia [16-18]. Furthermore, COMP has been shown to be upregulated after traumatic knee injury [19] and has been implicated in the pathogenesis of rheumatoid arthritis [20] and osteoarthritis (OA) [12,21]. During mouse development, COMP staining has been described around maturing articular chondrocytes [22], and during rat development it has been associated mainly with the growth plate [23]. Fang and colleagues [24] detected COMP as early as day 10 in murine development in the condensing mesenchyme, and later it was found in the growth plate and superficially in the developing joint cartilage. At the time of birth, COMP has been detected in the perichondrium, the periosteum, and the
Heat shock protein 70 level of synovial fluid in rheumatoid arthritis versus osteoarthritis: a comparative study
Gharibdoost F,Samadi F,Taghipoor R,Akbarian M
Tehran University Medical Journal , 2007,
Abstract: Background: Heat-shock proteins are part of a strictly controlled biological system that allows organisms to respond to environmental stresses. Different proinflammatory cytokines are present in the synovial tissue of rheumatoid arthritis patients. Such tissues respond to stress and induce heat-shock proteins. In addition, synovial cells are exposed to mechanical stress caused by joint motion. The effects of mechanical stress on the metabolism of the synovial cells may be substantial, even pathogenic. Heat-shock proteins are often implicated in the pathogenesis of rheumatoid arthritis. Here, we compare the levels of heat-shock protein 70 from the synovial fluid of rheumatoid arthritis and osteoarthritis patients.Methods: Synovial fluid samples from 34 rheumatoid arthritis patients and 34 osteoar-thritis patients were analyzed for heat-shock protein 70 by an ELISA method. Statistical analysis was performed using independent T-test and one-way ANOVA. Differences were considered statistically significant at p< 0.05.Results: The mean value of synovial fluid heat-shock protein 70 levels in rheumatoid arthritis patients was 156.30 ±128.51 and that of osteoarthritis patients was 14.98 ±11.58. The differences were statistically significant at p<0.0001. For seven rheumatoid arthritis patients suffering from mechanical knee pain, synovial fluid analysis revealed non-inflammatory effusion. The mean value of synovial fluid heat-shock protein 70 level in inflammatory synovial fluid of rheumatoid arthritis patients was significantly higher at 191±121.73 and that of non-inflammatory synovial fluid from rheumatoid arthritis patients was 21.93 ±10.06 (p< 0.05).Conclusion: The level of heat shock protein 70 is higher in inflammatory arthritis than in non-inflammatory arthritis. Considering that patients with rheumatoid arthritis are known to have a hypertrophic synovial-lining layer, and that heat-shock protein 70 is known to protect cells against a variety of toxic conditions as well as apoptotic death, further research is needed to determine if heat-shock protein 70 induction is a sign of significant changes in the cellular and tissue metabolism or is actively participating in the pathogenesis of rheumatoid arthritis.
MLN51 and GM-CSF involvement in the proliferation of fibroblast-like synoviocytes in the pathogenesis of rheumatoid arthritis
Jinah Jang, Dae-Seog Lim, Young-Eun Choi, Yong Jeong, Seung-Ah Yoo, Wan-Uk Kim, Yong-Soo Bae
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar2079
Abstract: Synovial tissue from healthy individuals consists of a single layer of synovial cells without infiltration of inflammatory cells. In rheumatoid synovial tissue, lymphocytes and macrophages are recruited and activated, and these activated macrophages release high concentrations of inflammatory cytokines. In response to these cytokines, synovial fibroblasts proliferate vigorously and form villous hyperplastic synovial tissues. These fibroblasts secrete inflammatory mediators, which further attract inflammatory cells and stimulate the growth of the synovial fibroblasts and vascular endothelial cells [1]. These activated macrophages and fibroblasts produce tissue-degrading proteinases [2]. Thus, invasive hyperplastic synovial tissue, termed pannus, is directly responsible for the structural and functional damage to the affected joints. Therapeutic intervention against rheumatoid arthritis (RA) could aim at any one of the aforementioned steps, but the driving mechanisms underlying this process are largely unknown. Impaired regulation of apoptosis has been associated with RA [3-5]; however, apoptosis of synovial cells has been identified in rheumatoid synovium [6,7], which suggests that synovial tissue hyperplasia may be a result of cell proliferation rather than apoptotic cell death [8-10].This study was initiated to address the molecular characterization of fibroblast-like synoviocyte (FLS) hyperproliferation in RA pathogenesis. We used cDNA microarray technology to identify genes related to the proliferation of RA FLSs. We found that the expression of the MLN51 (metastatic lymph node 51) gene was markedly enhanced in RA FLSs when cultured in the presence of the RA synovial fluid (SF). MLN51 was first identified in breast cancer cells, and the same investigators subsequently reported that MLN51 associates with exon junction complexes in the cell nucleus and remains stably associated with mRNA in the cytoplasm [11,12]. Recently, the interactions of MLN51 with other exon
Ganglioside GM3 Has an Essential Role in the Pathogenesis and Progression of Rheumatoid Arthritis  [PDF]
Yukinori Tsukuda, Norimasa Iwasaki, Naoki Seito, Masashi Kanayama, Naoki Fujitani, Yasuro Shinohara, Yasuhiko Kasahara, Tomohiro Onodera, Koji Suzuki, Tsuyoshi Asano, Akio Minami, Tadashi Yamashita
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040136
Abstract: Rheumatoid arthritis (RA), a chronic systemic inflammatory disorder that principally attacks synovial joints, afflicts over 2 million people in the United States. Interleukin (IL)-17 is considered to be a master cytokine in chronic, destructive arthritis. Levels of the ganglioside GM3, one of the most primitive glycosphingolipids containing a sialic acid in the structure, are remarkably decreased in the synovium of patients with RA. Based on the increased cytokine secretions observed in in vitro experiments, GM3 might have an immunologic role. Here, to clarify the association between RA and GM3, we established a collagen-induced arthritis mouse model using the null mutation of the ganglioside GM3 synthase gene. GM3 deficiency exacerbated inflammatory arthritis in the mouse model of RA. In addition, disrupting GM3 induced T cell activation in vivo and promoted overproduction of the cytokines involved in RA. In contrast, the amount of the GM3 synthase gene transcript in the synovium was higher in patients with RA than in those with osteoarthritis. These findings indicate a crucial role for GM3 in the pathogenesis and progression of RA. Control of glycosphingolipids such as GM3 might therefore provide a novel therapeutic strategy for RA.
RANTES and Chemotactic Activity in Synovial Fluids From Patients With Rheumatoid Arthritis and Osteoarthritis  [PDF]
Joanna Stanczyk,Marek L. Kowalski,Janina Grzegorczyk,Barbara Szkudlinska,Marzanna Jarzebska,Marek Marciniak,Marek Synder
Mediators of Inflammation , 2005, DOI: 10.1155/mi.2005.343
Abstract: A massive accumulation of inflammatory cells in synovial tissues is a major pathological feature of rheumatoid arthritis (RA). Neutrophiles dominate synovial fluid while rheumatoid synovium is infiltrated with mononuclear cells. Mechanisms regulating influx of particular subpopulations of leukocytes into articular cavity and synovium compartment are not completely defined. An increasing amount of data supports a crucial role of a C-C chemokine RANTES in the RA pathogenesis. Our objective is to evaluate chemotactic activity for neutrophils (NCA), lymphocytes (LCA), and monocytes (MoCA) in SFs obtained from patients with RA and osteoarthritis (OA). We also aimed to characterise the relation between chemotactic activity, RANTES, and percentage distribution of leukocytes in SF. SFs from 11 patients with RA and 6 with OA were included in the study. Modified microchamber Boyden method was employed to assess chemotactic activity. Cytological and biochemical analysis of SF was performed. RANTES was measured with ELISA. Rheumatoid SFs were rich in cells with predominance of neutrophiles while osteoarthritic fluids were lymphocytic. RA SFs were also characterised by increased lactoferrin level. Both NCA and LCA were higher in SF from patients with RA (62±12 and 24±6 cells/HPF, resp) as compared to patients with OA (23±6; P<.05 and 6±2 cells/HPF; P<0.05). The chemoattractive effect of RA SF was more pronounced on neutrophiles than on lymphocytes. RA SF expressed high RANTES levels (145±36pg/mL), while OA SF was characterised by only trace amount of this chemokine (2±1 pg/mL). We found positive correlation of RANTES with chemotactic activity for mononuclear cells (LCA
Osteo-Rheumatology: a new discipline?
Gerolamo Bianchi, Luigi Sinigaglia
Arthritis Research & Therapy , 2012, DOI: 10.1186/ar3708
Abstract: Since its origin, the meeting focused on the interactions between the bone tissue, the immune system and the cartilage in osteoarthritis, rheumatoid arthritis and spondyloarthropathies, always considering the two sides of the coin: the basic and clinical. In past years, as well as this year, specific sessions were dedicated to osteoarthritis (OA), rheumatoid arthritis (RA) and ankylosing spondylitis, respectively, with a starting session considering the general aspects of the topic. In this context, the bone damage as an early manifestation of arthritides, the systemic skeletal involvement in RA, the crucial role played by subchondral bone in the pathogenesis and progression of OA, the pathophysiology of glucocorticoids damage on the bone tissue, and the potential beneficial effects of newly approved agents such as bisphosphonates and biologics, but not only, were discussed.In 2011, the meeting has been named, for its first time, "Osteo-Rheumatology", thus implying the necessity of giving a more clear definition to topics presented and the issues raised. Even this year, experts in bone and rheumatic diseases interacted to improve our knowledge regarding the bone involvement in arthritis and to raise issues to be addressed in the future.
HLA DR4 subtype relationship with rheumatoid arthritis: a study on Iranian patients
Jamshidi AR,Tehrani Banihashemi SA,Salari AH,Taghipour R
Tehran University Medical Journal , 2009,
Abstract: "nBackground: There are several evidences that genetic factors besides environmental triggers have important role in initiating the rheumatoid arthritis (RA). The aim of this study was to investigate the association of rheumatoid arthritis with different subtypes of HLA DR4 in Iranian patients. "nMethods: In an un-matched case control study, 110 rheumatoid arthritis patients (case) and 56 knee osteoarthritis patients (control) of outpatient clinic in Shariati Hospital were entered to the study. After blood sampling from case and control groups, DNA was isolated by using salting-out method and HLA DR4 and its subtypes were detected. Association of HLA DR4 and its subtypes with rheumatoid arthritis, rheumatic factor and clinical manifestations of diseases was evaluated. "nResults: Eighty nine (80.9%) of rheumatoid arthritis patients were female and 21 were male. Thirty four of the RA patients (30.9%) and eleven subjects from the control group (19.6%) were HLA DR4 positive (p=0.12). The most frequent subtype of HLA DR4 in RA patients was 0404 and in control group was 0401 (p=0.03). There were not statistically significant association between HLA DR4 and age of disease onset, family history, morning stiffness and rheumatoid factor. Joint swelling and tenderness had association with HLA DR4 (p=0.04 and p=0.03). "nConclusion: Although there were no statistically significant association between rheumatoid arthritis and HLA DR4, but prevalence of this HLA was higher in patients than control. It is possible that in some ethnics, other HLAs may have role in pathogenesis of disease.
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