Prostaglandin E2 receptors EP1 and EP4 are up-regulated in rabbit chondrocytes by IL-1beta, but not by TNFalpha
Autor: | M. Angeles Alvarez-Soria, Gabriel Herrero-Beaumont, Emilio Calvo, Raquel Largo, Jesús Egido, Olga Sánchez-Pernaute |
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Rok vydání: | 2006 |
Předmět: |
medicine.medical_specialty
Necrosis Knee Joint Immunology Interleukin-1beta Chondrocytes Rheumatology Downregulation and upregulation Internal medicine Gene expression medicine Immunology and Allergy Animals Receptors Prostaglandin E RNA Messenger Prostaglandin E2 Receptor Cells Cultured biology business.industry Tumor Necrosis Factor-alpha Interleukin Receptors Prostaglandin E EP1 Subtype Up-Regulation Endocrinology Cyclooxygenase 2 biology.protein lipids (amino acids peptides and proteins) Tumor necrosis factor alpha Cyclooxygenase Rabbits medicine.symptom business Receptors Prostaglandin E EP4 Subtype medicine.drug |
Zdroj: | Rheumatology international. 27(10) |
ISSN: | 0172-8172 |
Popis: | 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. |
Databáze: | OpenAIRE |
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