ArticleRheumatology international2007
Prostaglandin E2 receptors EP1 and EP4 are up-regulated in rabbit chondrocytes by IL-1beta, but not by TNFalpha.
Article in Rheumatology international, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Exploring the mechanism of action ofHeliyon · 2024Article
- Review
- Fasitibant prevents the bradykinin and interleukin 1β synergism on prostaglandin E₂ release and cyclooxygenase 2 expression in human fibroblast-like synoviocytes.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- Bradykinin and B₂ receptor antagonism in rat and human articular chondrocytes.British journal of pharmacology · 2011Article
- Neuroprotection in a rabbit model of intraventricular haemorrhage by cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha inhibition.Brain : a journal of neurology · 2010Article
- A suppressive effect of prostaglandin EOpen access rheumatology : research and reviews · 2009Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E2 (PGE2) exerts its actions through the binding of the high affinity EP receptors. We wanted to evaluate the regulation of EP1 and EP4, and the expression of cyclooxygenase (COX)-2, main enzyme responsible for PGE2 synthesis in inflammatory situations, in healthy rabbit chondrocytes stimulated with inflammatory mediators locally increased during osteoarthritis. Articular chondrocytes obtained from healthy rabbits were stimulated with interleukin (IL)-1beta (0.1-100 u/ml) or tumour necrosis factor (TNF)alpha (100 ng/ml). Where indicated, cells were preincubated with non-steroidal antiinflammatory drugs (NSAIDs) (10(-6) M) to inhibit PGE2 synthesis. IL-1beta induced a dose and time-dependent increase in EP1, EP4 and COX-2 expression. However, TNFalpha presence did not induce a significant modification in EP1, EP4 or COX-2 gene expression at any time of study. NSAID presence significantly inhibited PGE2 release but did not modify the EP receptors or COX-2 expression induced by IL-1beta. Our results indicate that EP1 and EP4 receptors, and COX-2 are up-regulated in IL-1beta-stimulated chondrocytes, while no significant modifications are observed in TNFalpha-stimulated cells. NSAIDs were unable to modify the expression of these mediators induced by IL-1beta. Therefore, the increase in PGE2 synthesis, induced by IL-1beta, does not seem to mediate the increase in EP receptor expression, in rabbit chondrocytes.
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