Developmental Mechanisms in Articular Cartilage Degradation in Osteoarthritis

Tchetina, Elena V.

doi:10.1155/2011/683970

Cited by 81 publications

(81 citation statements)

References 224 publications

(259 reference statements)

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“…A change in the behavior of chondrocytes in the articular cartilage is believed to play an important role during OA pathogenesis (18)(19)(20). We conditionally deleted Mig-6 in the chondrogenic cells and, to our surprise, found that the joint phenotype only partially recapitulated the OA-like disorder of mice with complete deletion of Mig-6.…”

Section: Discussionmentioning

confidence: 79%

“…The core pathological changes in OA include articular cartilage degradation and formation of osteophyte (also known as bony outgrowth) and subchondral cysts (17)(18)(19)(20), which can all be observed in the Mig-6-deficient synovial joints (11). Chondrocytes in the articular cartilage synthesize many cartilage proteins for building the extracellular matrix (ECM) network that is responsible for withstanding biomechanical force.…”

mentioning

confidence: 99%

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Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation

Staal

Williams

Beier

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance Mitogen-inducible gene 6 (Mig-6) was found to be an important factor in maintaining joint homeostasis, and its loss in mice results in the development of an osteoarthritis (OA)-like disorder in multiple synovial joints. However, it was unclear in what cells Mig-6 was expressed and what cells were causal for developing the OA-like phenotype. Here we report that Mig-6 is uniquely expressed in the cells surrounding entire surface of the synovial joint, including chondrocytes in the superficial zone of the articular cartilage and in the meniscus, and synovial lining cells. We found that although chondrocytes play a critical role in developing the OA-like disorder in the knees, other cell types are likely required for full development of the Mig-6–deficient joint phenotype.

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Section: Discussionmentioning

confidence: 79%

mentioning

confidence: 99%

Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation

Staal

Williams

Beier

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Different from most tissues, articular cartilage is not traversed by blood vessels, nerves or lymphatic vessels (reviewed in: Findlay, 2007). While the extracellular matrix has a low metabolism of collagen, the turnover rate of aggrecan is relatively high (Tchetina, 2011) with a calculated half-life of about 4 years (reviewed in: Sivan et al, 2014). It has been stressed by Ahlqvist et al (1989) that cartilage requires a considerable amount of energy, which has been determined on the basis of oxygen consumption, with 0.01 µL O 2 /h per mg dry joint cartilage, a value which is in the range of the one measured for carotid body tissue (Starlinger and Lübbers, 1976).…”

Section: Introductionmentioning

confidence: 99%

Artificial cartilage bio-matrix formed of hyaluronic acid and Mg2+-polyphosphate

Wang¹,

Ackermann²,

Tolba³

et al. 2016

eCM

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Here we show that inorganic polyphosphate (polyP), a polyanionic metabolic regulator consisting of multiple phosphate residues linked by energy-rich phosphoanhydride bonds, is present in the synovial fluid. In a biomimetic approach, to enhance cartilage synthesis and regeneration, we prepared amorphous polyP microparticles with Mg 2+ as counterions. The particles were characterised by X-ray diffraction (XRD), energy-dispersive X-ray (EDX) and Fourier transformed infrared spectroscopic (FTIR) analyses. Similar particles were obtained after addition of Mg 2+ ions to a solution containing hyaluronic acid, as a major component of the synovial fluid, and soluble NapolyP. The viscous paste-like material formed, composed of globular microparticles with diameter of 400 nm, strongly promoted the adhesion of chondrocytes and caused a significant upregulation of the expression of the genes encoding collagen type 3A1, as a marker for chondrocyte differentiation, and SOX9, a transcription factor that regulates chondrocyte differentiation and proliferation. The expression level of the collagen type 3A1 gene was also enhanced by exposure of chondrocytes to synovial fluid that was found to contain polyP with a size of about 80 phosphate residues. This stimulatory effect was abolished after pre-incubation of the synovial fluid with the polyP degrading alkaline phosphatase. We propose a strategy for treatment of joint dysfunctions caused by osteoarthritis based on the application of amorphous Mg 2+ -polyP microparticles that prevent calcium crystal formation in the synovial fluid using scavenging Ca -polyP to hyaluronic acid at the cartilage surface.

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“…Though the mechanism underlying the development OA is yet to be understood, several biochemichal pathways have been found to be associated with the development of OA (Tchetina, 2011;Valdes and Spector, 2009). …”

Section: Introductionmentioning

confidence: 99%

Association of Polymorphism in Growth and Differentiation Factor 5 Gene With Osteoarthritis Knee

Mishra¹,

Sanghi²,

Sharma³

et al. 2013

American Journal of Biochemistry and Biotechnology

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The present study investigated to identify the association of polymorphism in GDF-5 gene with osteoarthritis in North Indian population. In a case-control study, 300 cases with knee osteoarthritis and an equal number of age and gender matched healthy controls were included. Cases were diagnosed using the ACR Guidelines of Knee Osteoarthritis (KOA). Clinical symptoms were assessed with the knee specific WOMAC index and VAS for knee pain. The severity of disease was determined by radiological KL grades (Kellgren Lawren). The variant genotype of GDF-5 was found to be present at significantly higher frequency in cases than in controls, resulting in about 1.79 fold increase in risk to OA. Genotype distributions of the GDF-5 also showed significant association of variant allele with clinical score of OA patients. An association between the+104T/C GDF5 polymorphism with knee OA and clinical symptom of OA in Indian population further demonstrate a strong genetic influence of this SNP in KOA.

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Developmental Mechanisms in Articular Cartilage Degradation in Osteoarthritis

Cited by 81 publications

References 224 publications

Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation

Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation

Artificial cartilage bio-matrix formed of hyaluronic acid and Mg2+-polyphosphate

Association of Polymorphism in Growth and Differentiation Factor 5 Gene With Osteoarthritis Knee

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