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Renal Division (B.D.B., U.A., K.A.H.), Departments of Medicine and Cell Biology, Barnes-Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110
Address all correspondence and requests for reprints to: Brian Bennett, Renal Division, Barnes-Jewish Hospital, Washington University School of Medicine, 216 South Kingshighway, Mailstop #90–32-648, St. Louis, Missouri 63110. E-mail: bbennett{at}im.wustl.edu
Osteoclasts "sense" elevated extracellular calcium, which leads to cytoskeletal changes that may be linked to phospholipase C (PLC) activation and the associated rise in intracellular calcium ([Ca2+]i). Since PLC is linked to transient receptor potential channels (trp), we hypothesized that receptor activated calcium influx due to this channel type would be activated by osteoclasts sensing [Ca2+]e. We found that high [Ca2+]e induced similar intracellular Ca2+ rises in chicken osteoclasts with or without intracellular Ca2+ store depletion by either TPEN or thapsigargin, thus defining store-insensitive Ca2+ influx. This store-insensitive calcium sensing component was blocked by the PLC antagonist U73122. Also, the calcium channel inhibitor SKF 96365, a blocker of store-independent trp-like channels, was effective in inhibiting calcium sensing in the presence of thapsigargin. Thus, a store-independent component of calcium sensing was associated with ion channels linked to PLC. Since receptor activated transient receptor potential (trp) family cation channels open in a PLC-dependent and store-independent manner, we suggest that receptor operated channels are activated in osteoclasts stimulated by high extracellular Ca2+.
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