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J Biol Chem, Vol. 274, Issue 39, 27776-27785, September 24, 1999
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From the Lysophosphatidic acid (LPA), together with
sphingosine 1-phosphate, is a bioactive lipid mediator that acts on
G-protein-coupled receptors to evoke multiple cellular responses,
including Ca2+ mobilization, modulation of adenylyl
cyclase, and mitogen-activated protein (MAP) kinase activation. In this
study, we isolated a human cDNA encoding a novel G-protein-coupled
receptor, designated EDG7, and characterized it as a cellular receptor
for LPA. The amino acid sequence of the EDG7 protein is 53.7 and 48.8%
identical to those of the human functional LPA receptors EDG2 and EDG4, respectively, previously identified. LPA (oleoyl) but not other lysophospholipids induced an increase in the
[Ca2+]i of EDG7-overexpressing Sf9 cells.
Other LPA receptors, EDG4 but not EDG2, transduced the Ca2+
response by LPA when expressed in Sf9 cells. LPAs with an
unsaturated fatty acid but not with a saturated fatty acid induced an
increase in the [Ca2+]i of EDG7-expressing
Sf9 cells, whereas LPAs with both saturated and unsaturated
fatty acids elicited a Ca2+ response in Sf9 cells
expressing EDG4. In EDG7- or EDG4-expressing Sf9 cells, LPA
stimulated forskolin-induced increase in intracellular cAMP levels,
which was not observed in EDG2-expressing cells. In PC12 cells, EDG4
but not EDG2 or EDG7 mediated the activation of MAP kinase by LPA.
Neither the EDG7- nor EDG4-transduced Ca2+ response or cAMP
accumulation was inhibited by pertussis toxin. In conclusion, the
present study demonstrates that EDG7, a new member of the EDG family of
G-protein-coupled receptors, is a specific LPA receptor that shows
distinct properties from known cloned LPA receptors in ligand
specificities, Ca2+ response, modulation of adenylyl
cyclase, and MAP kinase activation.
Graduate School of Pharmaceutical Sciences,
The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan, the Faculty of Pharmaceutical Sciences, Science
University of Tokyo, 12 Ichigaya-Funagawara-machi, Shinjuku-ku, Tokyo
162-0826, Japan, the ** Department of Biology, Faculty of Science,
Ochanomizu University, 2-1-1, Otsuka, Bunkyo-ku, Tokyo 112-8610, Japan,
and the § Laboratory of Cellular Biochemistry, The Institute
of Physical and Chemical Research (RIKEN), 2-1, Hirosawa, Wako-shi,
Saitama 351-0198, Japan
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