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(2)

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Abstract #6320 Published in IGR 3-2

Functional pharmacological evidence for EP2 and EP4 prostanoid receptors in immortalized human trabecular meshwork and non-pigmented ciliary epithelial cells

Crider JY; Sharif NA
Journal of Ocular Pharmacology and Therapeutics 2001; 17: 35-46

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The aim of these studies was to characterize the molecular pharmacology of the prostanoid receptors positively coupled to stimulation of adenylyl cyclase activity in immortalized human trabecular meshwork (TM-3) cells and to compare these results with that of the receptors in immortalized human nonpigmented epithelial (NPE) cells. In general, the TM-3 and NPE cells showed a similar profile with respect to their responses to various prostaglandin (PG) receptor agonists. The rank order of potency (EC₅₀; means ± SEM) for these compounds in the TM-3 cells was: PGE₂ (124 ± 21 nM) > 13,14-dihydro-PGE₁ (430 ± 110 nM) = PGE₁ (522 ± 345 nM) > 11-deoxy-PGE₁ (1063 ± 118 nM) = 16,16-dimethyl-PGE₂ (1776 ± 460 nM) = butaprost (1920 ± 527 nM) >> PGD₂ = PGI₂ = PGF_2α (n = 3-12). While the agonist profile indicated the presence of EP₂ receptors, the effects of the EP₄ receptor antagonists suggested the additional expression of EP₄ receptors in both of these cells. Thus, the EP₄ receptor antagonist, AH23848B, at a concentration of 30 μm, caused a dextral shift in the PGE₂ concentration-response curves in both TM-3 and NPE cells coupled with a 20-28% decrease in the maximal response of PGE₂, indicating apparent noncompetitive antagonism profiles. The antagonist potency of AH23848B in these cells was: Kb = 38.4 ± 14.8 μm and 23.5 ± 4.5 μm; -log Kb = 4.7. The other EP₄ receptor antagonist, AH22921 (-log Kb = 4.1-4.7), was weaker than AH23848B. Taken together, these pharmacological studies have shown than TM-3 and NPE cells apparently contain functional EP₂ and EP₄ prostanoid receptors positively coupled to adenylyl cyclase.

Dr J.Y. Crider, Molecular Pharmacology Unit, Alcon Research, Ltd., Fort Worth, TX 76134, USA. Julie.Crider@AlconLabs.com

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Classification:

2.5 Meshwork (Part of: 2 Anatomical structures in glaucoma)
3.3 Immunohistochemistry (Part of: 3 Laboratory methods)

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