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PMID: 11156559 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Potentiation of cytokine induction of group IIA phospholipase A(2) in rat mesangial cells by ATP and adenosine via the A2A adenosine receptor.

British journal of pharmacology ·Vol. 132 ·No. 1 ·2001-01-00 ·Pages 37-46

Scholz-Pedretti K, Pfeilschifter J, Kaszkin M

Abstract

1. In rat mesangial cells extracellular nucleotides were found to increase arachidonic acid release by a cytosolic phospholipase A(2) through the P2Y(2) purinergic receptor. 2. In this study we investigated the effects of ATP and UTP on interleukin-1ss (IL-1ss)-induced mRNA expression and activity of group IIA phospholipase A(2) (sPLA(2)-IIA) in rat mesangial cells. 3. Treatment of cells for 24 h with extracellular ATP potentiated IL-1ss-stimulated sPLA(2)-IIA induction, whereas UTP had no effect. 4. We obtained the following evidence that the P2Y(2) receptor is not involved in the potentiation of sPLA(2)-IIA induction: (i) ATP-gamma-S had no enhancing effect; (ii) suramin, a P(2) receptor antagonist, did not inhibit ATP-mediated potentiation; (iii) inhibition of degradation of extracellular nucleotides by the 5'-ectonucleotidase inhibitor AOPCP did not enhance sPLA(2)-IIA induction and (iv) adenosine deaminase treatment completely abolished the ATP-mediated potentiation of sPLA(2)-IIA induction. 5. In contrast, treatment of mesangial cells with adenosine or the A2A receptor agonist CGS 21680 mimicked the effects of ATP in enhancing IL-1ss-stimulated sPLA(2)-IIA induction, whereas the specific A2A receptor antagonist ZM 241385 completely abolished the potentiating effect of ATP or adenosine. 6. The protein kinase A inhibitor Rp-8-Br-cyclic AMPS dose-dependently inhibited the enhancing effect of ATP or adenosine indicating the participation of an adenosine receptor-mediated cyclic AMP-dependent signalling pathway. 7. These data indicate that ATP mediates proinflammatory long-term effects in rat mesangial cells via its degradation product adenosine through the A2A receptor resulting in potentiation of sPLA(2)-IIA induction.

MeSH Terms
5'-Nucleotidase/antagonists & inhibitors,metabolism Adenosine/metabolism,pharmacology Adenosine Deaminase/pharmacology Adenosine Triphosphate/analogs & derivatives,metabolism,pharmacology Animals Blotting, Northern Cells, Cultured Enzyme Induction Enzyme Inhibitors/pharmacology Glomerular Mesangium/cytology,drug effects,metabolism Group II Phospholipases A2 Interleukin-1/pharmacology Phospholipases A/biosynthesis Purinergic P2 Receptor Antagonists RNA, Messenger/biosynthesis Rats Receptor, Adenosine A2A Receptors, Purinergic P1/drug effects Signal Transduction/drug effects Suramin/pharmacology Triazines/pharmacology Triazoles/pharmacology Uridine Triphosphate/metabolism,pharmacology Vasodilator Agents/pharmacology
Chemicals
Enzyme Inhibitors Interleukin-1 Purinergic P2 Receptor Antagonists RNA, Messenger Receptor, Adenosine A2A Receptors, Purinergic P1 Triazines Triazoles Vasodilator Agents ZM 241385 adenosine 5'-O-(3-thiotriphosphate) Suramin Adenosine Triphosphate Phospholipases A Group II Phospholipases A2 5'-Nucleotidase Adenosine Deaminase Adenosine Uridine Triphosphate
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Scholz-Pedretti K
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai-7, D-60590 Frankfurt am Main, Germany.
Pfeilschifter J
Kaszkin M
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Article Info
Journal
British journal of pharmacology
Abbr.
Br J Pharmacol
ISSN
0007-1188
DOI
10.1038/sj.bjp.0703774
Published
2001-01-00
Pages
37-46
Language
English
Region
England
NLM ID
7502536
PMCID
PMC1572532
Subset
IM
External Links
PubMed source DOI: 10.1038/sj.bjp.0703774 PMC Full Text View journal details
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