Altered pain perception and inflammatory response in mice lacking prostacyclin receptor

Takahiko Murata, Fumitaka Ushikubi, Toshiyuki Matsuoka, Masakazu Hirata, Atsushi Yamasaki, Yukihiko Sugimoto, Atsushi Ichikawa, Yoshiya Aze, Takashi Tanaka, Nobuaki Yoshida, Akinori Ueno, Sachiko Oh-ishi and Shuh Narumiya ()
Additional contact information
Takahiko Murata: Faculty of Medicine
Fumitaka Ushikubi: Faculty of Medicine
Toshiyuki Matsuoka: Faculty of Medicine
Masakazu Hirata: Faculty of Medicine
Atsushi Yamasaki: Faculty of Pharmaceutical Sciences, Kyoto University
Yukihiko Sugimoto: Faculty of Pharmaceutical Sciences, Kyoto University
Atsushi Ichikawa: Faculty of Pharmaceutical Sciences, Kyoto University
Yoshiya Aze: Fukui Institute for Safety Research, Ono Pharmaceutical Company
Takashi Tanaka: Research Institute Osaka Medical Center for Maternal and Child Health
Nobuaki Yoshida: Research Institute Osaka Medical Center for Maternal and Child Health
Akinori Ueno: School of Pharmaceutical Sciences, Kitasato University
Sachiko Oh-ishi: School of Pharmaceutical Sciences, Kitasato University
Shuh Narumiya: Faculty of Medicine

Nature, 1997, vol. 388, issue 6643, 678-682

Abstract: Abstract Prostanoids are a group of bioactive lipids working as local mediators1 and include D, E, F and I types of prostaglandins (PGs) and thromboxanes. Prostacyclin (PGI2) acts on platelets and blood vessels to inhibit platelet aggregation and to cause vasodilatation, and is thought to be important for vascular homeostasis2. Aspirin-like drugs, including indomethacin, which inhibit prostanoid biosynthesis, suppress fever, inflammatory swelling and pain, and interfere with female reproduction, suggesting that prostanoids are involved in these processes1,3, although it is not clear which prostanoid is the endogenous mediator of a particular process. Prostanoids act on seven-transmembrane-domain receptors which are selective for each type4. Here we disrupt the gene for the prostacyclin receptor5 in mice by using homologous recombination. The receptor-deficient mice are viable, reproductive and normotensive. However, their susceptibility to thrombosis is increased, and their inflammatory and pain responses are reduced to the levels observed in indomethacin-treated wild-type mice. Our results establish that prostacyclin is an antithrombotic agent in vivo and provide evidence for its role as a mediator of inflammation and pain.

Date: 1997
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DOI: 10.1038/41780

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