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

التفاصيل البيبلوغرافية
المؤلفون الرئيسيون:	Burleigh, A, Chanalaris, A, Saklatvala, J, Vincent, T
التنسيق:	Conference item
منشور في:	BioMed Central 2012

مواد مشابهة

MECHANICAL LOAD DRIVES INFLAMMATORY GENE EXPRESSION AND DISEASE IN MURINE OA
حسب: Burleigh, A, وآخرون
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IL18 IS SECRETED UPON JOINT INJURY AND IS A KEY PATHOGENIC CYTOKINE IN MURINE OSTEOARTHRITIS
حسب: Vincent, T, وآخرون
منشور في: (2014)

Joint immobilization prevents murine osteoarthritis and reveals the highly mechanosensitive nature of protease expression in vivo.
حسب: Burleigh, A, وآخرون
منشور في: (2012)

ADAMTS4 and ADAMTS5 are upregulated early in the DMM model of murine OA
حسب: Burleigh, A, وآخرون
منشور في: (2009)

PARTIAL JOINT IMMOBILISATION PROTECTS AGAINST OA AND REVEALS DISTINCT BIOMECHANICAL THRESHOLDS IN THE JOINT
حسب: Burleigh, A, وآخرون
منشور في: (2010)

TSG‐6 is weakly chondroprotective in murine OA but does not account for FGF2‐mediated joint protection
حسب: Zhu, L, وآخرون
منشور في: (2020)

The role of biomechanical factors in OA development
حسب: Burleigh, A, وآخرون
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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
حسب: Papadopoulou, A, وآخرون
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Cyclic mechanical load causes global translational arrest in articular chondrocytes: a process which is partially dependent upon PKR phosphorylation.
حسب: Lomas, C, وآخرون
منشور في: (2011)

Cyclic mechanical load causes global translational arrest in articular chondrocytes: a process which is partially dependent upon PKR phosphorylation
حسب: C Lomas, وآخرون
منشور في: (2011-09-01)

Regulation of nerve growth factor in the articular cartilage causes pain in murine OA
حسب: Driscoll, C, وآخرون
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Fibroblast growth factor 2 drives changes in gene expression following injury to murine cartilage in vitro and in vivo.
حسب: Chong, K, وآخرون
منشور في: (2013)

Accelerated disease in a surgical model of murine OA in mice lacking FGF-2
حسب: Chia, S, وآخرون
منشور في: (2007)

CARTILAGE INJURY REGULATES NERVE GROWTH FACTOR (NGF) IN VTTRO AND IN VIVO AND DRIVES PAINFUL BEHAVIOUR IN MURINE OA
حسب: Driscoll, C, وآخرون
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Transcriptional analysis of micro-dissected articular cartilage in post-traumatic murine osteoarthritis.
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Structural changes in the collagen network of joint tissues in late stages of murine OA
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Creation of an activin A conditional knockout mouse for OA research
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The dependence of FGF2 on murine cartilage injury responses
حسب: Chong, K, وآخرون
منشور في: (2011)

JNK-dependent modulation of the protease secretome profile of osteoarthritic cartilage
حسب: Ismail, H, وآخرون
منشور في: (2018)

CCL2 and CCR2 regulate pain-related behaviour and early gene expression in post-traumatic murine osteoarthritis but contribute little to chondropathy
حسب: Miotla Zarebska, J, وآخرون
منشور في: (2016)

Fibroblast growth factor 2 is an intrinsic chondroprotective agent that suppresses ADAMTS-5 and delays cartilage degradation in murine osteoarthritis.
حسب: Chia, S, وآخرون
منشور في: (2009)

Acute and sustained molecular changes in synovial fluid following acute knee injury mirror the murine joint injury response
حسب: Watt, F, وآخرون
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Enzymatic Construction of Protein Polymer/Polyprotein Using OaAEP1 and TEV Protease
حسب: Yibing Deng, وآخرون
منشور في: (2020-04-01)

Differential inflammatory gene expression patterns in JNK2 knockout mice in response to IL1, cartilage injury and surgically induced osteoarthritis
حسب: Ismail, HM, وآخرون
منشور في: (2016)

Interleukin-17 is a potential contributor to the inflammatory environment in the OA joint
حسب: Mimpen, J, وآخرون
منشور في: (2019)

CTGF IS RELEASED FROM THE PERICELLULAR MATRIX OF ARTICULAR CARTILAGE UPON MECHANICAL INJURY, AND CONTROLS THE BIOAVAILABILITY OF TGF beta
حسب: Tang, X, وآخرون
منشور في: (2014)

CTGF is released from the pericellular matrix of articular cartilage upon mechanical injury, and promotes the bioavailability of TGF beta
حسب: Tang, X, وآخرون
منشور في: (2014)

Prognostic characterization of OAS1/OAS2/OAS3/OASL in breast cancer
حسب: Yujie Zhang, وآخرون
منشور في: (2020-06-01)

Evolution of organic aerosol mass spectra upon heating: implications for OA phase and partitioning behavior
حسب: C. D. Cappa, وآخرون
منشور في: (2011-03-01)

NIGHT-TIME SPLINTING OF THE DISTAL INTERPHALANGEAL JOINT REDUCES PAIN AND IMPROVES EXTENSION AT THE JOINT: RESULTS FROM THE SPLINT-OA STUDY
حسب: Watt, F, وآخرون
منشور في: (2013)

Loss of murine Gfi1 causes neutropenia and induces osteoporosis depending on the pathogen load and systemic inflammation.
حسب: Sven Geissler, وآخرون
منشور في: (2018-01-01)

Association Between the Morphology of Proximal Tibiofibular Joint and the Presence of Knee OA
حسب: Xin-Zheng Qi, وآخرون
منشور في: (2020-12-01)

Load-dependent effects of apelin on murine cardiomyocytes
حسب: Peyronnet, R, وآخرون
منشور في: (2017)

OAS1, OAS2 and OAS3 restrict intracellular M. tb replication and enhance cytokine secretion
حسب: Gina Leisching, وآخرون
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Treatment of murine osteoarthritis with TrkAd5 reveals a pivotal role for nerve growth factor in non-inflammatory joint pain.
حسب: McNamee, K, وآخرون
منشور في: (2010)

Activation of mitogen activated Protein Kinases (MAPKs) and gene induction upon explantation in articular cartilage from wild type and FGF-2(-/-) mice
حسب: Chong, K, وآخرون
منشور في: (2009)

High systemic bone mineral density increases the risk of incident knee OA and joint space narrowing, but not radiographic progression of existing knee OA: the MOST study.
حسب: Nevitt, M, وآخرون
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ASSOCIATIONS OF INTERFERON GENE POLYMORPHISMS OAS-1, OAS-3, PKR WITH CHRONIC VIRAL HEPATITIS C
حسب: V. A. Bychkov, وآخرون
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Production and Characterization of an Extracellular Acid Protease from Thermophilic Brevibacillus sp. OA30 Isolated from an Algerian Hot Spring
حسب: Mohamed Amine Gomri, وآخرون
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