Interleukin-1β enhances the response of human articular chondrocytes to extracellular ATP

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

doi:10.1016/0167-4889(92)90099-w

Cited by 21 publications

(14 citation statements)

References 33 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). Chondrocytes are now know to express multiple P2 receptor subtypes including the P2X1, P2X2, P2X3, P2X4, P2X7, P2Y1 and P2Y2 receptors (Koolpe et al, 1999;Knight et al, 2009;Varani et al, 2008b;Kudirka et al, 2007).…”

Section: P2 Receptor Expression By Chondrocytesmentioning

confidence: 99%

“…Other reported effects of purinergic signalling include increased chondrocyte differentiation (Fodor et al, 2009), elevated fibroblast growth factor-induced proliferation (Kaplan et al, 1996;Koolpe et al, 1997) and increased responsiveness to IL-1β and TNF-α (Caswell et al, 1992;Leong et al, 1993).…”

Section: Functional Effects Of P2 Receptor Signalling In Chondrocytesmentioning

confidence: 99%

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The role of purinergic signalling in the musculoskeletal system

Orriss

2015

Autonomic Neuroscience

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Section: P2 Receptor Expression By Chondrocytesmentioning

confidence: 99%

Section: Functional Effects Of P2 Receptor Signalling In Chondrocytesmentioning

confidence: 99%

The role of purinergic signalling in the musculoskeletal system

Orriss

2015

Autonomic Neuroscience

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“…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). Finally, there are metabotropic (P2Y) receptors on the membranes of articular tissues.…”

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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“…The following year, ATP was shown to simulate PGE 2 production from articular chondrocytes [296]. P2 receptors were later identified on human articular chondrocytes that were responsive to UTP as well as ATP [297]. Subsequently, P2U (P2Y 2 and/or P2Y 4 ) receptors were identified on sheep chondrocytes [298,299].…”

Section: P2 Receptor Expression By Chondrocytesmentioning

confidence: 99%

“…The response of human articular chondrocytes to ATP is enhanced by IL-1β [297] and TNF-α [318,319]. Activation of P2Y receptors also leads to elevated fibroblast growth factor-induced proliferation [298,299].…”

Section: P2 Receptor Expression By Chondrocytesmentioning

confidence: 99%

Purinergic signalling in the musculoskeletal system

Burnstock

Arnett

Orriss

2013

Purinergic Signalling

111

114

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It is now widely recognised that extracellular nucleotides, signalling via purinergic receptors, participate in numerous biological processes in most tissues. It has become evident that extracellular nucleotides have significant regulatory effects in the musculoskeletal system. In early development, ATP released from motor nerves along with acetylcholine acts as a cotransmitter in neuromuscular transmission; in mature animals, ATP functions as a neuromodulator. Purinergic receptors expressed by skeletal muscle and satellite cells play important pathophysiological roles in their development or repair. In many cell types, expression of purinergic receptors is often dependent on differentiation. For example, sequential expression of P2X5, P2Y 1 and P2X2 receptors occurs during muscle regeneration in the mdx model of muscular dystrophy. In bone and cartilage cells, the functional effects of purinergic signalling appear to be largely negative. ATP stimulates the formation and activation of osteoclasts, the bone-destroying cells. Another role appears to be as a potent local inhibitor of mineralisation. In osteoblasts, the bone-forming cells, ATP acts via P2 receptors to limit bone mineralisation by inhibiting alkaline phosphatase expression and activity. Extracellular ATP additionally exerts significant effects on mineralisation via its hydrolysis product, pyrophosphate. Evidence now suggests that purinergic signalling is potentially important in several bone and joint disorders including osteoporosis, rheumatoid arthritis and cancers. Strategies for future musculoskeletal therapies might involve modulation of purinergic receptor function or of the ecto-nucleotidases responsible for ATP breakdown or ATP transport inhibitors.

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Interleukin-1β enhances the response of human articular chondrocytes to extracellular ATP

Cited by 21 publications

References 33 publications

The role of purinergic signalling in the musculoskeletal system

The role of purinergic signalling in the musculoskeletal system

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

Purinergic signalling in the musculoskeletal system

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