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Receptor-operated osteoclast calcium sensing
B D Bennett1, U Alvarez, K A Hruska
1Renal Division, Departments of Medicine and Cell Biology, Barnes-Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Endocrinology
|April 24, 2001
Summary
Osteoclasts sense high extracellular calcium via store-insensitive calcium influx, involving phospholipase C (PLC) and transient receptor potential (TRP) channels. This suggests receptor-operated channels activate in osteoclasts responding to elevated calcium levels.
Area of Science:
- Cell Biology
- Calcium Signaling
- Skeletal Biology
Background:
- Osteoclasts, crucial for bone resorption, respond to extracellular calcium ([Ca(2+)](e)).
- Phospholipase C (PLC) activation and intracellular calcium ([Ca(2+)](i)) rise are implicated in this response.
- Transient receptor potential (TRP) channels are linked to PLC and calcium influx.
Purpose of the Study:
- To investigate the role of TRP channels in calcium sensing by osteoclasts.
- To determine if calcium influx is PLC-dependent and store-independent in osteoclasts sensing high extracellular calcium.
Main Methods:
- Utilized chicken osteoclasts to study calcium influx.
- Manipulated intracellular calcium stores using TPEN or thapsigargin.
- Applied PLC antagonist (U73122) and TRP channel inhibitor (SKF 96365).
Main Results:
- High extracellular calcium induced store-insensitive intracellular calcium rises in osteoclasts.
- This calcium sensing was blocked by U73122, indicating PLC involvement.
- SKF 96365 also inhibited calcium sensing, suggesting TRP channel activation.
Conclusions:
- Osteoclasts exhibit a store-independent calcium influx mechanism linked to PLC.
- Receptor-operated TRP channels are likely activated by elevated extracellular calcium in osteoclasts.