共查询到20条相似文献,搜索用时 31 毫秒
1.
Andrew D Cook Christine M De Nardo Emma L Braine Amanda L Turner Ross Vlahos Kerrie J Way S Kaye Beckman Jason C Lenzo John A Hamilton 《Arthritis research & therapy》2010,12(2):R37
Introduction
Urokinase-type plasminogen activator (u-PA) has been implicated in fibrinolysis, cell migration, latent cytokine activation, cell activation, T-cell activation, and tissue remodeling, all of which are involved in the development of rheumatoid arthritis. Previously, u-PA has been reported to play a protective role in monoarticular arthritis models involving mBSA as the antigen, but a deleterious role in the systemic polyarticular collagen-induced arthritis (CIA) model. The aim of the current study is to determine how u-PA might be acting in systemic arthritis models. 相似文献2.
Adrienn Angyal Colt Egelston Tamás Kobezda Katalin Olasz Anna László Tibor T Glant Katalin Mikecz 《Arthritis research & therapy》2010,12(2):R44
Introduction
Inflammatory joint destruction in rheumatoid arthritis (RA) may be triggered by autoantibodies, the production of which is supported by autoreactive T cells. Studies on RA and animal models of the disease suggest that T cells recruited in the joints can locally initiate or propagate arthritis. Herein, we investigated the role of joint-homing versus lymphoid organ-homing T cells in the development of proteoglycan-induced arthritis (PGIA), an autoimmune model of RA. 相似文献3.
Joana RF Abreu Daphne de Launay Marjolein E Sanders Aleksander M Grabiec G Marleen van de Sande Paul P Tak Kris A Reedquist 《Arthritis research & therapy》2009,11(4):R121-13
Introduction
Fibroblast-like synoviocytes (FLS) from rheumatoid arthritis (RA) patients share many similarities with transformed cancer cells, including spontaneous production of matrix metalloproteinases (MMPs). Altered or chronic activation of proto-oncogenic Ras family GTPases is thought to contribute to inflammation and joint destruction in RA, and abrogation of Ras family signaling is therapeutic in animal models of RA. Recently, expression and post-translational modification of Ras guanine nucleotide releasing factor 1 (RasGRF1) was found to contribute to spontaneous MMP production in melanoma cancer cells. Here, we examine the potential relationship between RasGRF1 expression and MMP production in RA, reactive arthritis, and inflammatory osteoarthritis synovial tissue and FLS. 相似文献4.
Hyun-Mi Choi Yeon-Ah Lee Sang-Hoon Lee Seung-Jae Hong Dae-Hyun Hahm Sang-Yun Choi Hyung-In Yang Myung Chul Yoo Kyoung Soo Kim 《Arthritis research & therapy》2009,11(6):R161-10
Introduction
The role of adiponectin in the pathogenesis of arthritis is still controversial. This study was performed to examine whether adiponectin is involved in joint inflammation and destruction in rheumatoid arthritis (RA) in relation to the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs). 相似文献5.
Introduction
Macrophage migration inhibitory factor (MIF) is one of key regulators in acute and chronic immune-inflammatory conditions including rheumatoid arthritis (RA). We examined the effect of MIF on osteoclastogenesis, which is known to play a crucial role in bone destruction in RA. 相似文献6.
Introduction
There is an ever-increasing need for animal models to evaluate efficacy and safety of new therapeutics in the field of rheumatoid arthritis (RA). Particularly for the early preclinical evaluation of human-specific biologicals targeting the progressive phase of the disease, there is a need for relevant animal models. In response to this requirement we set out to develop a model of collagen-induced arthritis (CIA) in a small-sized nonhuman primate species (300 to 400 g at adult age); that is, the common marmoset (Callithrix jacchus). 相似文献7.
John M Davis III Keith L Knutson John A Skinner Michael A Strausbauch Cynthia S Crowson Terry M Therneau Peter J Wettstein Eric L Matteson Sherine E Gabriel 《Arthritis research & therapy》2012,14(1):R24-11
Introduction
Progression of joint damage despite appropriate therapy remains a significant problem for patients with rheumatoid arthritis (RA). This study was undertaken to identify profiles of immune response that correlate with radiographic joint damage as a first step toward the discovery of new pathogenic mechanisms of joint destruction in RA. 相似文献8.
Hekmat K Jacobsson L Nilsson JÅ Petersson IF Robertsson O Garellick G Turesson C 《Arthritis research & therapy》2011,13(2):R67
Introduction
One aim of modern pharmacologic treatment in rheumatoid arthritis (RA) is to prevent joint destruction and reduce the need for surgery. Our purpose was to investigate secular trends in the incidence of primary total hip and knee arthroplasties in a well defined sample of patients with RA. 相似文献9.
Bäcklund A Holmdahl M Mattsson R Håkansson K Lindström V Nandakumar KS Grubb A Holmdahl R 《Arthritis research & therapy》2011,13(2):R54
Introduction
Collagen-induced arthritis (CIA) is a mouse model for rheumatoid arthritis (RA) and is induced after immunization with type II collagen (CII). CIA, like RA, is an autoimmune disease leading to destruction of cartilage and joints, and both the priming and inflammatory phases have been suggested to be dependent on proteases. In particular, the cysteine proteases have been proposed to be detrimental to the arthritic process and even immunomodulatory. A natural inhibitor of cysteine proteases is cystatin C. 相似文献10.
Michael K Boettger Johannes Leuchtweis Diana Kümmel Mieczyslaw Gajda Rolf Br?uer Hans-Georg Schaible 《Arthritis research & therapy》2010,12(4):R140
Introduction
Interleukin-6 (IL-6) is a key player in systemic arthritis, involved in inflammation and joint destruction. IL-6 signalling has also been revealed in nerve cells. Recently, IL-6 and in particular IL-6 together with its soluble IL-6 receptor (sIL-6R) were shown to induce a long-lasting robust sensitization of joint nociceptors for mechanical stimuli which was difficult to reverse, suggesting that IL-6 signalling plays a significant role in the generation and maintenance of arthritic pain. Here we tested in a preclinical model of arthritis, antigen-induced arthritis (AIA) in the rat, whether systemic or local neutralization of IL-6/sIL-6R complexes with soluble glycoprotein 130 (sgp130) alters arthritic pain and how sgp130 influences the inflammatory process in AIA. 相似文献11.
Andreas K Lübke C Häupl T Dehne T Morawietz L Ringe J Kaps C Sittinger M 《Arthritis research & therapy》2008,10(1):R9
Background
Rheumatoid arthritis (RA) is a chronic, inflammatory and systemic autoimmune disease that leads to progressive cartilage destruction. Advances in the treatment of RA-related destruction of cartilage require profound insights into the molecular mechanisms involved in cartilage degradation. Until now, comprehensive data about the molecular RA-related dysfunction of chondrocytes have been limited. Hence, the objective of this study was to establish a standardized in vitro model to profile the key regulatory molecules of RA-related destruction of cartilage that are expressed by human chondrocytes. 相似文献12.
Shoko Toyama Naoto Tamura Kazuhiko Haruta Takeo Karakida Shigeyuki Mori Tetsuo Watanabe Takao Yamori Yoshinari Takasaki 《Arthritis research & therapy》2010,12(3):R92
Introduction
Targeting joint destruction induced by osteoclasts (OCs) is critical for management of patients with rheumatoid arthritis (RA). Since phosphoinositide 3-kinase (PI3-K) plays a critical role in osteoclastogenesis and bone resorption, we examined the effects of ZSTK474, a novel phosphoinositide 3-kinase (PI3-K)-specific inhibitor, on murine OCs in vitro and in vivo. 相似文献13.
Ekwall AK Eisler T Anderberg C Jin C Karlsson N Brisslert M Bokarewa MI 《Arthritis research & therapy》2011,13(2):R40
Introduction
Activated fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) share many characteristics with tumour cells and are key mediators of synovial tissue transformation and joint destruction. The glycoprotein podoplanin is upregulated in the invasive front of several human cancers and has been associated with epithelial-mesenchymal transition, increased cell migration and tissue invasion. The aim of this study was to investigate whether podoplanin is expressed in areas of synovial transformation in RA and especially in promigratory RA-FLS. 相似文献14.
Noreen Pundt Marvin A Peters Christina Wunrau Simon Strietholt Carsten Fehrmann Katja Neugebauer Christine Seyfert Frans van Valen Thomas Pap Ingmar Meinecke 《Arthritis research & therapy》2009,11(1):R16-10
Introduction
The rheumatoid arthritis (RA) synovium is characterised by the presence of an aggressive population of activated synovial fibroblasts (RASFs) that are prominently involved in the destruction of articular cartilage and bone. Accumulating evidence suggests that RASFs are relatively resistant to Fas-ligand (FasL)-induced apoptosis, but the data concerning tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) have been conflicting. Here, we hypothesise that the susceptibility of RASFs to receptor-mediated apoptosis depends on the proliferation status of these cells and therefore analysed the cell cycle dependency of FasL- and TRAIL-induced programmed cell death of RASFs in vitro. 相似文献15.
Lee HM Sugino H Aoki C Shimaoka Y Suzuki R Ochi K Ochi T Nishimoto N 《Arthritis research & therapy》2011,13(3):R89
Introduction
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis that progresses to destruction of cartilage and bone. Bone marrow (BM) cells have been shown to contribute to this pathogenesis. In this study, we compared differentially expressed molecules in BM cells from RA and osteoarthritis (OA) patients and analyzed abnormal regulatory networks to identify the role of BM cells in RA. 相似文献16.
Adipue IA Wilcox JT King C Rice CA Shaum KM Suard CM Brink Et Miller SD McMahon EJ 《Arthritis research & therapy》2011,13(4):R114
Introduction
Mouse models of rheumatoid arthritis (RA) have proven critical for identifying genetic and cellular mechanisms of the disease. Upon discovering mice in our breeding colony that had spontaneously developed inflamed joints reminiscent of RA, we established the novel IIJ (inherited inflamed joints) strain. The purpose of this study was to characterize the histopathological, clinical, genetic and immunological properties of the disease. 相似文献17.
Chang BY Huang MM Francesco M Chen J Sokolove J Magadala P Robinson WH Buggy JJ 《Arthritis research & therapy》2011,13(4):R115
Introduction
The aim was to determine the effect of the Bruton tyrosine kinase (Btk)-selective inhibitor PCI-32765, currently in Phase I/II studies in lymphoma trials, in arthritis and immune-complex (IC) based animal models and describe the underlying cellular mechanisms. 相似文献18.
Engvall IL Svensson B Tengstrand B Brismar K Hafström I;Better Anti-Rheumatic FarmacO Therapy Study Group 《Arthritis research & therapy》2008,10(6):R128
Introduction
Patients with rheumatoid arthritis (RA) have an increased frequency of osteoporosis, mainly because of increased bone resorption. Reduction of disease activity is suggested to reduce bone remodelling. It might also be possible that prednisolone treatment could cause this effect because prednisolone has been shown to arrest the development of joint destruction in early RA. Therefore, we examined the effects of low-dose prednisolone on serum concentrations of bone remodelling markers and insulin-like growth factor-1 (IGF-1) in RA patients in relation to bone mineral density. 相似文献19.
Bianca Miterski Susanne Drynda Gundula B?schow Wolfram Klein Joachim Oppermann J?rn Kekow J?rg Thomas Epplen 《BMC genetics》2004,5(1):2
Background
Rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA) are complex multifactorial diseases caused by environmental influences and an unknown number of predisposing genes. The present study was undertaken in order to investigate association of polymorphisms in candidate genes with RA and JRA in German subjects. 相似文献20.
Maria D Mjaavatten Till Uhlig Anne J Haugen Halvor Nygaard Göran Sidenvall Knut Helgetveit Tore K Kvien 《Arthritis research & therapy》2009,11(5):R146-8