Evidence for the presence of P2-purinoceptors at the surface of human articular chondrocytes in monolayer culture

Caswell, Amanda; Leong, Weng S.; Russell, R. G. G.

doi:10.1016/0304-4165(91)90054-k

Cited by 49 publications

(34 citation statements)

References 37 publications

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“…The following year, ATP was found to increase the production of PGE2 from articular chondrocytes (Caswell et al, 1991). Several early studies reported that chondrocytes were responsive to UTP as well as ATP indicating the presence of P2Y receptors (Caswell et al, 1992;Kaplan et al, 1996;Koolpe et al, 1997).…”

Section: P2 Receptor Expression By Chondrocytesmentioning

confidence: 94%

The role of purinergic signalling in the musculoskeletal system

Orriss

2015

Autonomic Neuroscience

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Section: P2 Receptor Expression By Chondrocytesmentioning

confidence: 94%

The role of purinergic signalling in the musculoskeletal system

Orriss

2015

Autonomic Neuroscience

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“…Chondrocytes have ATP receptors in their membranes (Caswell et al, 1991). Since extracellular ATP Fig.…”

Section: Dna Contentmentioning

confidence: 99%

Adenosine 5′‐triphosphate promotes mineralization in differentiating chick limb‐bud mesenchymal cell cultures

Boskey

Doty

Binderman

1994

Microscopy Res & Technique

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When chick limb-bud mesenchymal cells are plated in micromass culture, they differentiate to form a mineralizable cartilage matrix. Previous studies have demonstrated that, when the total inorganic phosphate concentration of the medium is adjusted to 3-4 mM by adding inorganic phosphate to the basal medium, the mineralized matrix formed resembles that of chick calcified cartilage in ovo. When the high-energy phosphates adenosine 5'-triphosphate (ATP) or creatine phosphate are used as supplements in place of inorganic phosphate, the mineralized matrix as analyzed by electron microscopy and Fourier transform infrared microscopy is also similar to that in ovo. This is in marked contrast to the mineralized matrix formed in the presence of 2.5-5 mM beta-glycerophosphate, where mineral deposition is random and mineral crystal sizes in general are larger. This is also in contrast to the known ability of ATP to inhibit mineral deposition in solution in the absence of cells. In the differentiating mesenchymal cell culture system, ATP does not alter the rate of cell proliferation (DNA content), the rate of matrix synthesis (3H-leucine uptake), the mean crystallite length, or the rate of mineral deposition (45Ca uptake) when contrasted with cultures supplemented with inorganic phosphate. However, ATP does increase the mineral to matrix ratio, especially around the edge of the culture, where a type I collagen matrix is presented. It is suggested that ATP promotes mineral deposition by providing a high-energy phosphate source, which may be used to phosphorylate extracellular matrix proteins and to regulate calcium flux through cell membranes.

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“…This is supported by the finding that the synovial fluids of patients affected by OA or RA contain high concentrations of ATP (6). Leong et al (7,8) reported that ATP triggered the degradation of cultured explants of bovine nasal cartilage and stimulated PGE 2 production by articular chondrocytes. IL-1␤ and TNF-␣ both interact synergistically with extracellular ATP (9,10).…”

mentioning

confidence: 99%

Concomitant Recruitment of ERK1/2 and p38 MAPK Signalling Pathway Is Required for Activation of Cytoplasmic Phospholipase A2via ATP in Articular Chondrocytes

Bérenbaum¹,

Humbert²,

Béréziat³

et al. 2003

Journal of Biological Chemistry

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Extracellular ATP is a pro-inflammatory mediator involved in the release of prostaglandin from articular chondrocytes, but little is known about its effects on intracellular signaling. ATP triggered the rapid release of prostaglandin E 2 (PGE 2 ) by acting on P2Y 2 receptors in rabbit articular chondrocytes. We have explored the signaling events involved in this synthesis. ATP significantly increased arachidonic acid production, which involved the activation of the 85-kDa cytosolic phospholipase A 2 (cPLA 2 ) but not a secreted form of PLA 2 , as demonstrated by various PLA 2 inhibitors and translocation experiments. We also showed that ATP induced the phosphorylation of p38 and ERK1/2 mitogen-activatedprotein kinases (MAPKs). Both PD98059, an inhibitor of the ERK pathway, and SB203580, an inhibitor of p38 MAPK, completely inhibited the ATP-induced release of PGE 2 . Finally, dominant-negative plasmids encoding p38 and ERK transfected alone into the cells impaired the ATP-induced release of PGE 2 to about the same extent as both plasmids transfected together. These results suggest that PGE 2 production induced by ATP requires the activation of both ERK1/2 and p38 MAPKs. Thus, ATP acts via P2Y 2 -purine receptors to recruit cPLA 2 by activating both ERK1/2 and p38 MAPKs and stimulates the release of PGE 2 from articular chondrocytes.

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Evidence for the presence of P2-purinoceptors at the surface of human articular chondrocytes in monolayer culture

Cited by 49 publications

References 37 publications

The role of purinergic signalling in the musculoskeletal system

The role of purinergic signalling in the musculoskeletal system

Adenosine 5′‐triphosphate promotes mineralization in differentiating chick limb‐bud mesenchymal cell cultures

Concomitant Recruitment of ERK1/2 and p38 MAPK Signalling Pathway Is Required for Activation of Cytoplasmic Phospholipase A2via ATP in Articular Chondrocytes

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