Pathogenic protease expression in murine OA is critically dependent upon mechanical joint loading

Pathogenic protease expression in murine OA is critically dependent upon mechanical joint loading

Bibliografski detalji
Glavni autori:	Burleigh, A, Chanalaris, A, Saklatvala, J, Vincent, T
Format:	Conference item
Izdano:	BioMed Central 2012

Slični predmeti

MECHANICAL LOAD DRIVES INFLAMMATORY GENE EXPRESSION AND DISEASE IN MURINE OA
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IL18 IS SECRETED UPON JOINT INJURY AND IS A KEY PATHOGENIC CYTOKINE IN MURINE OSTEOARTHRITIS
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Joint immobilization prevents murine osteoarthritis and reveals the highly mechanosensitive nature of protease expression in vivo.
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ADAMTS4 and ADAMTS5 are upregulated early in the DMM model of murine OA
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PARTIAL JOINT IMMOBILISATION PROTECTS AGAINST OA AND REVEALS DISTINCT BIOMECHANICAL THRESHOLDS IN THE JOINT
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TSG‐6 is weakly chondroprotective in murine OA but does not account for FGF2‐mediated joint protection
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The role of biomechanical factors in OA development
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TSG‐6 Is Weakly Chondroprotective in Murine OA but Does not Account for FGF2‐Mediated Joint Protection
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Fibromodulin and tenascin N are potential biomarkers of post-traumatic OA
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Cyclic mechanical load causes global translational arrest in articular chondrocytes: a process which is partially dependent upon PKR phosphorylation.
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Cyclic mechanical load causes global translational arrest in articular chondrocytes: a process which is partially dependent upon PKR phosphorylation
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Regulation of nerve growth factor in the articular cartilage causes pain in murine OA
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Fibroblast growth factor 2 drives changes in gene expression following injury to murine cartilage in vitro and in vivo.
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Accelerated disease in a surgical model of murine OA in mice lacking FGF-2
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Transcriptional analysis of micro-dissected articular cartilage in post-traumatic murine osteoarthritis.
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JNK-dependent modulation of the protease secretome profile of osteoarthritic cartilage
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CCL2 and CCR2 regulate pain-related behaviour and early gene expression in post-traumatic murine osteoarthritis but contribute little to chondropathy
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Fibroblast growth factor 2 is an intrinsic chondroprotective agent that suppresses ADAMTS-5 and delays cartilage degradation in murine osteoarthritis.
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Differential inflammatory gene expression patterns in JNK2 knockout mice in response to IL1, cartilage injury and surgically induced osteoarthritis
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CTGF IS RELEASED FROM THE PERICELLULAR MATRIX OF ARTICULAR CARTILAGE UPON MECHANICAL INJURY, AND CONTROLS THE BIOAVAILABILITY OF TGF beta
od: Tang, X, i dr.
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CTGF is released from the pericellular matrix of articular cartilage upon mechanical injury, and promotes the bioavailability of TGF beta
od: Tang, X, i dr.
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Interleukin-17 is a potential contributor to the inflammatory environment in the OA joint
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NIGHT-TIME SPLINTING OF THE DISTAL INTERPHALANGEAL JOINT REDUCES PAIN AND IMPROVES EXTENSION AT THE JOINT: RESULTS FROM THE SPLINT-OA STUDY
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Loss of murine Gfi1 causes neutropenia and induces osteoporosis depending on the pathogen load and systemic inflammation.
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Load-dependent effects of apelin on murine cardiomyocytes
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OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion
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