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Vol. 63, Issue 4, 777-783, April 2003
Institute of Interdisciplinary Research, Institute of Biology and
Molecular Medicine, Université Libre de Bruxelles, Gosselies,
Belgium (B.R., F.W., D.F., S.S., J.-M.B.), Laboratory of
Physiopathology, School of Medicine, Université Libre de
Bruxelles, Brussels, Belgium (E.G., R.B.), Department of Physiology,
Katholiek Universiteit of Leuven, Leuven, Belgium (W.V.D.), Laboratory
of Medical Chemistry, Erasme Hospital, Université Libre de
Bruxelles, Brussels, Belgium (J.-M.B.)
The P2Y4 receptor is responsive to UTP in human and to ATP
and UTP in rodents. With the aim of identifying its pharmacotherapeutic interest, we generated P2Y4-null mice by a classic
gene targeting method. The proportion of genotypes was consistent with
X-linked Mendelian transmission. Gene inactivation was checked by the
complete disappearance of P2Y4 receptor mRNA from liver,
stomach, and intestine. The P2Y4-null mice had a grossly
normal behavior, growth, and reproduction. Chloride secretion by the
jejunal epithelium was assessed in Ussing chambers by the measurement
of the short circuit current in the presence of phlorizin. We show here
that the UTP- and ATP-induced chloride secretory responses observed in
wild-type mice are abolished in P2Y4-null mice. This is the
first clearcut demonstration of a biological role of the
P2Y4 receptor.
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