Phenotypic Characterization of Inflammatory Cells from Osteoarthritic Synovium and Synovial Fluids

Haynes, Mark K.; Hume, Eric; Smith, J. Bruce

doi:10.1006/clim.2002.5283

Cited by 96 publications

(86 citation statements)

References 48 publications

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“…Interferon-γ (IFN-γ) is a cytokine that is critical for innate and adaptive immunity against viral and intracellular bacterial infections. T cells from OA synovial fluids express an activated phenotype and synthesized IFN-γ, supporting the hypothesis that inflammatory cells play a significant role in OA disease progression and chronicity (39).…”

Section: Discussionsupporting

confidence: 60%

Obtain osteoarthritis related molecular signature genes through regulation network

Wang

et al. 2011

Mol Med Report

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Abstract. Osteoarthritis (OA), also known as degenerative joint disease or osteoarthrosis, is the most common form of arthritis. OA occurs when cartilage in the joints wears down over time. We used the GSE1919 series to identify potential genes that correlated to OA. The aim of our study was to obtain a molecular signature of OA through the regulation network based on differentially expressed genes. From the result of regulation network construction in OA, a number of transcription factors (TFs) and pathways closely related to OA were linked by our method. Peroxisome proliferator-activated receptor γ also arises as hub nodes in our transcriptome network and certain TFs containing CEBPD, EGR2 and ETS2 were shown to be related to OA by a previous study.

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Section: Discussionsupporting

confidence: 60%

Obtain osteoarthritis related molecular signature genes through regulation network

Wang

et al. 2011

Mol Med Report

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“…Inflammatory cells, cytokines and growth factors that are not normally present in the cartilage matrix are found in OA patients [437,464].…”

Section: Metalloproteinases and Osteoarthritismentioning

confidence: 99%

Metalloproteinases and Metalloproteinase Inhibitors in Age-Related Diseases

Gargiulo¹,

Gamba²,

Poli³

et al. 2014

CPD

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Degradation of the extracellular matrix is an important feature of embryonic development, morphogenesis, angiogenesis, tissue repair and remodeling. It is precisely regulated under physiological conditions, but when dysregulated it becomes a cause of many diseases, including atherosclerosis, osteoarthritis, diabetic vascular complications, and neurodegeneration. Various types of proteinases are implicated in extracellular matrix degradation, but the major enzymes are considered to be metalloproteinases such as matrix metalloproteinases (MMPs) and disintegrin and metalloproteinase domain (ADAMs) that include ADAMs with a thrombospondin domain (ADAMTS).This review discusses involvement of the major metalloproteinases in some age-related chronic diseases, and examines what is currently known about the beneficial effects of their inhibitors, used as new therapeutic strategies for treating or preventing the development and progression of these diseases.

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“…Increased release of COX-2 in subchondral osteoblasts is thought to play a role in stimulating bone resorption [139,140]. Furthermore, the abovementioned mediators may additionally enhance neovascularization at the osteoarthritic synovial tissue [141,142].…”

Section: Osteoarthritismentioning

confidence: 99%

Angiogenesis and chronic inflammation: cause or consequence?

2007

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Evidence has been gathered regarding the association between angiogenesis and inflammation in pathological situations. These two phenomena have long been coupled together in many chronic inflammatory disorders with distinct etiopathogenic origin, including psoriasis, rheumatoid arthritis, Crohn's disease, diabetes, and cancer. Lately, this concept has further been substantiated by the finding that several previously established non-inflammatory disorders, such as osteoarthritis and obesity, display both inflammation and angiogenesis in an exacerbated manner. In addition, the interplay between inflammatory cells, endothelial cells and fibroblasts in chronic inflammation sites, together with the fact that inflammation and angiogenesis can actually be triggered by the same molecular events, further strengthen this association. Therefore, elucidating the underlying cellular and molecular mechanisms that gather together the two processes is mandatory in order to understand their synergistic effect, and to develop new therapeutic approaches for the management of these disorders that cause a great deal of discomfort, disability, and in some cases death.

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Phenotypic Characterization of Inflammatory Cells from Osteoarthritic Synovium and Synovial Fluids

Cited by 96 publications

References 48 publications

Obtain osteoarthritis related molecular signature genes through regulation network

Obtain osteoarthritis related molecular signature genes through regulation network

Metalloproteinases and Metalloproteinase Inhibitors in Age-Related Diseases

Angiogenesis and chronic inflammation: cause or consequence?

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