'Calcium-activated' intracellular calcium elevation: a novel mechanism of osteoclast regulation.
The osteoclast is unique in its capacity to resorb bone. An unbalanced increase in this activity causes osteoporosis, a crippling bone disease that poses a major public health problem. Despite this, our understanding of osteoclast regulation is very limited. Calcitonin is the only known physiological inhibitor of osteoclast function. We demonstrate here for the first time that the concentration of calcium ions at the resorptive site directly regulates osteoclast function by modulating the intracellular free calcium concentration. This represents an important feedback mechanism of osteoclast control.
Cell Biology Unit, Royal Postgraduate Medical School, London, UK.
M
M
Zaidi
H K
HK
Datta
A
A
Patchell
B
B
Moonga
I
I
MacIntyre
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001862:Bone Resorption; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D004987:Ethers / Q000494:pharmacology; D015759:Ionomycin; D007700:Kinetics; D008274:Magnesium / Q000494:pharmacology; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D051381:Rats
D004987:Ethers; D015759:Ionomycin; D009532:Nickel; D000135:Acid Phosphatase; D008274:Magnesium; D009543:Nifedipine; D011188:Potassium; D002118:Calcium