Jacob Bell
New Member
Nariman Balenga1, Ralf Schröder2, Julia Kargl1, Wolfgang Platzer1, Stefanie Blättermann2, Ãkos Heinemann1, Evi Kostenis2 and Maria Waldhoer1 email
1 Institute of Experimental and Clinical Pharmacology, Medical University of Graz, 8010 Graz, Austria
2 Section Molecular, Cellular and Pharmacobiology, Institute for Pharmaceutical Biology, University of Bonn, 53115 Bonn, Germany
author email corresponding author email
from 15th Scientific Symposium of the Austrian Pharmacological Society (APHAR) Joint meeting with the Hungarian Society of Experimental and Clinical Pharmacology (MFT) and the Slovenian Pharmacological Society (SDF)
Graz, Austria. 19-21 November 2009
BMC Pharmacology 2009, 9(Suppl 2):A3doi:10.1186/1471-2210-9-S2-A3
The electronic version of this abstract is the complete one and can be found online at: BioMed Central | Full text | GPR55: signaling pathways and functions
Published: 12 November 2009
© 2009 Balenga et al; licensee BioMed Central Ltd.
Background
We have recently shown that the G protein-coupled receptor 55 (GPR55) mediates intracellular effects of cannabinoids and other, non-cannabinoid ligands in addition to the classical cannabinoid 1 (CB1) and 2 (CB2) receptors. Here we show different signaling pathways triggered by GPR55 in response to a panel of its agonists. In addition the cytoskeleton rearrangement mediated by GPR55 is investigated.
Methods
HEK-293 cells stably expressing the GPR55 receptor were characterized in terms of signaling properties. To this end, FLEX calcium release, reporter gene, dynamic mass redistribution (DMR) and phalloidin actin staining assays have been performed.
Results
Here we show that GPR55 is activated by lysophosphatidylinositol (LPI), AM251, SR141716A (rimonabant) and AM281. GPR55 activation induces intracellular calcium release, NF-κB, NFAT and CREB activation. Stimulation of GPR55 induces F-actin formation under the control of Gα13, RhoA and ROCK. We also show the suitability of Corning® Epic® DMR assay for GPR55 ligand screening.
Conclusion
GPR55 as the novel cannabinoid receptor triggers distinct signaling pathways in response to LPI and some classical CB1 receptor antagonists. Stress fiber formation mediated by GPR55 might show the function of this receptor in vivo.
Source: GPR55: signaling pathways and functions
1 Institute of Experimental and Clinical Pharmacology, Medical University of Graz, 8010 Graz, Austria
2 Section Molecular, Cellular and Pharmacobiology, Institute for Pharmaceutical Biology, University of Bonn, 53115 Bonn, Germany
author email corresponding author email
from 15th Scientific Symposium of the Austrian Pharmacological Society (APHAR) Joint meeting with the Hungarian Society of Experimental and Clinical Pharmacology (MFT) and the Slovenian Pharmacological Society (SDF)
Graz, Austria. 19-21 November 2009
BMC Pharmacology 2009, 9(Suppl 2):A3doi:10.1186/1471-2210-9-S2-A3
The electronic version of this abstract is the complete one and can be found online at: BioMed Central | Full text | GPR55: signaling pathways and functions
Published: 12 November 2009
© 2009 Balenga et al; licensee BioMed Central Ltd.
Background
We have recently shown that the G protein-coupled receptor 55 (GPR55) mediates intracellular effects of cannabinoids and other, non-cannabinoid ligands in addition to the classical cannabinoid 1 (CB1) and 2 (CB2) receptors. Here we show different signaling pathways triggered by GPR55 in response to a panel of its agonists. In addition the cytoskeleton rearrangement mediated by GPR55 is investigated.
Methods
HEK-293 cells stably expressing the GPR55 receptor were characterized in terms of signaling properties. To this end, FLEX calcium release, reporter gene, dynamic mass redistribution (DMR) and phalloidin actin staining assays have been performed.
Results
Here we show that GPR55 is activated by lysophosphatidylinositol (LPI), AM251, SR141716A (rimonabant) and AM281. GPR55 activation induces intracellular calcium release, NF-κB, NFAT and CREB activation. Stimulation of GPR55 induces F-actin formation under the control of Gα13, RhoA and ROCK. We also show the suitability of Corning® Epic® DMR assay for GPR55 ligand screening.
Conclusion
GPR55 as the novel cannabinoid receptor triggers distinct signaling pathways in response to LPI and some classical CB1 receptor antagonists. Stress fiber formation mediated by GPR55 might show the function of this receptor in vivo.
Source: GPR55: signaling pathways and functions
