Identification and Characterization of a Sodium/Calcium Exchanger, NCX-1, in Osteoclasts and Its Role in Bone Resorption Baljit S. Moonga,* Robert Davidson,† Li Sun,* Olugbenga A. Adebanjo,* James Moser,‡ Mohammad Abedin,§ Neeha Zaidi,* Christopher L.-H. Huang, and Mone Zaidi* ,1 *Mount Sinai Bone Program, Departments of Medicine and Geriatrics, Mount Sinai School of Medicine, and Bronx Veteran’s Affairs (VA) Geriatric Research Education and Clinical Center (GRECC), New York, New York; David Kriser School of Dentistry, New York University, New York, New York; Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania; §VA Medical Center, Philadelphia, Pennsylvania; and Physiological Laboratory, University of Cambridge, Cambridge, United Kingdom Received April 17, 2001 We provide the first demonstration for a Na /Ca 2 ex- changer, NCX-1, in the osteoclast. We speculate that by using Na exchange, NCX-1 couples H extrusion with Ca 2 fluxes during bone resorption. Microspectrofluo- rimetry of fura-2-loaded osteoclasts revealed a rapid and sustained, but reversible, cytosolic Ca 2 elevation upon Na withdrawal. This elevation was abolished by the cytosolic introduction (by gentle permeabilization) of a highly specific Na /Ca 2 exchange inhibitor peptide, XIP, but not its inactive analogue, sXIP. Confocal mi- croscopy revealed intense plasma membrane immuno- fluorescence with an isoform-specific monoclonal anti- NCX-1 antibody applied to gently permeabilized osteoclasts. Electrophysiological studies using excised outside-in membrane patches showed a low- conductance, Na -selective, dichlorobenzamil-sensitive, amiloride-insensitive channel that we tentatively as- signed as being an NCX. Finally, to examine for physio- logical relevance, an osteoclast resorption (pit) assay was performed. There was a dramatic reduction of bone resorption following NCX-1 inhibition by dichloroben- zamil and XIP (but not with S-XIP). Together, the results suggest that a functional NCX, likely NCX-1, is involved in the regulation of osteoclast cytosolic Ca 2 and bone resorption. © 2001 Academic Press Key Words: Na /Ca 2 exchange; osteoclasts; osteopo- rosis; bone resorption. The osteoclast is unique in that it is exposed to high levels of ambient Ca 2+ in the millimolar range [1]. Mechanisms exist through which rising ambient Ca 2+ concentrations are ‘sensed’ and transduced into intra- cellular Ca 2+ signals that regulate osteoclastic bone resorption [2, 3]. These responses are mediated through type 2 ryanodine receptor-gated Ca 2+ channels expressed at the plasma membrane [4]. We are, how- ever, unclear of mechanisms by which resorbed Ca 2+ is extruded to restore cytosolic Ca 2+ to basal levels. A Ca 2+ -ATPase has been identified on the osteoclast’s dorsal surface; however, little is known of alternative or parallel mechanisms of osteoclast Ca 2+ extrusion [5]. The primary functional role of Na + flux in the oste- oclast has typically been associated with H + exchange [6 –9]. Active osteoclasts involved in the resorptive phase of bone remodeling show a massive H + extrusion via a V-type H + -ATPase [10]. This step is essential for bone resorption. Changes in intracellular pH resulting from active proton pumping are readily corrected by a Cl - channel, a Cl - /HCO 3 - exchanger, and an amiloride- sensitive Na + /H + exchanger [6, 11–14]. We report func- tional, electrophysiological and immunochemical evi- dence for a Na + /Ca 2+ exchanger, likely an NCX-1, in the osteoclast. We hypothesize that, as in cardiac muscle, osteoclastic NCX-1 might couple with the Na + /H + ex- changer to assist in the regulation of cytosolic Ca 2+ [15]. This would mean that in addition to Ca 2+ -ATPase [5], there is a second mechanism for Ca 2+ extrusion following Ca 2+ influx through the surface ryanodine receptor/ extracellular Ca 2+ sensor [2, 4]. Unlike Ca 2+ -ATPase, however, this mechanism is linked to the proton extru- sion that is a primary determinant of the rate and extent of bone resorption. MATERIALS AND METHODS Microspectrofluorimetric measurements of cytosolic Ca 2+ . Osteo- clasts were freshly isolated as described previously [2]. Coverslips containing freshly isolated cells washed in -MEM and treated with 1 To whom correspondence should be addressed at Mount Sinai Bone Program, P.O. Box 1055, Endocrinology, Mount Sinai School of Medicine, One Gustave Levy Place, New York. NY 10029. Fax: 212-426-8312. E-mail: mone.zaidi@mssm.edu. Biochemical and Biophysical Research Communications 283, 770 –775 (2001) doi:10.1006/bbrc.2001.4870, available online at http://www.idealibrary.com on 770 0006-291X/01 $35.00 Copyright © 2001 by Academic Press All rights of reproduction in any form reserved.