2. Academic Validation
  3. Protein kinase A-dependent coupling of mouse prostacyclin receptors to Gi is cell-type dependent

Protein kinase A-dependent coupling of mouse prostacyclin receptors to Gi is cell-type dependent

  • Eur J Pharmacol. 2003 Aug 1;474(1):7-13. doi: 10.1016/s0014-2999(03)02006-5.
Kevin B S Chow 1,  Robert L Jones,  Helen Wise
Affiliations

Affiliation

  • 1 Department of Pharmacology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR, China.
PMID: 12909190 DOI: 10.1016/s0014-2999(03)02006-5
Abstract

The ability of the prostacyclin (IP) receptor agonist cicaprost to activate Gs-, Gq/11- and Gi-mediated cell signalling pathways has been examined in Chinese hamster ovary (CHO) cells and human embryonic kidney 293 (HEK 293) cells expressing the cloned human (hIP) or mouse (mIP) prostacyclin receptor, and compared with data from NG108-15 and SK-N-SH cells that endogenously express rat/mouse and human IP receptors, respectively. Cicaprost stimulated [3H]cyclic AMP production with EC50 values of 1.5-22 nM, and stimulated [3H]inositol phosphate production (EC50 values 49-457 nM) in all but the SK-N-SH cells. Cicaprost failed to inhibit forskolin-stimulated [3H]cyclic AMP production in any of these cell lines. Therefore, although both human and mouse IP receptors couple to Gs and Gq/11-mediated signalling pathways in a cell type-dependent manner, we could find no evidence for IP receptor coupling to Gi.

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