Lysophosphatidylcholine transduces ca2+ signaling via the platelet
-activating factor receptor in macrophages.
Ogita, Teruhiko, Yuji Tanaka, Takashi Nakaoka, Rumiko Matsuoka, Yuji
Kira, Motonao Nakamura, Takao Shimizu, and Toshiro Fujita.
Laboratory of Cardiovascular Research, Fourth Department of
Internal Medicine; Department of Biochemistry, Faculty of
Medicine,University of Tokyo, Tokyo 112; Tokyo Women's Medical
College, Tokyo 162; and Division of Cardiology, Showa General
Hospital, Kodaira City, Tokyo 187, Japan
APStracts 3:0285H, 1996.
To clarify the molecular mechanism underlying the
lysophosphatidylcholine (LPC) signaling, we studied the effect of LPC
on the intracellular free calcium concentration ([Ca2+]i) in murine
peritoneal macrophages. LPC, when added alone, induced biphasic
elevation of [Ca2+]i, which consisted of a rapid increase followed by
sustained elevation. LPC, when added with equimolar cholesterol,
induced only the rapid increase in ([Ca2+]i), which was blocked by
WEB 2086, a selective platelet-activating factor (PAF) receptor
antagonist. These results suggest LPC exerts a specific calcium
signaling. The sustained elevation reflected the cell lysis. Further,
we confirmed its pathway in a more specific manner using cloned PAF
receptors expressed in Chinese hamster ovary cells. LPC induced an
elevation of [Ca2+]i in a concentration-dependent manner only when
the PAF receptor had been expressed, and the elevation of [Ca2+]i was
blocked by WEB 2086. Taken together, LPC transduces Ca2+ signaling
via the PAF receptor. Activation of the PAF receptor by LPC may
indicate its novel important role in the pathogenesis of
atherosclerosis.
Received 4 March 1996; accepted in final form 3 July 1996.
APS Manuscript Number H210-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996