Extracellular Ca2+ sensing by the osteoclast.
An increasing number of cell types appear to detect changes in the extracellular Ca2+ concentration and and accordingly modify their function. We review recent evidence for the existence and function of such a mechanism in the osteoclast. Elevated external [Ca2+] in the mM range reduces bone resorption and results in motile changes in the cells. These changes may partly result from elevations of cytosolic [Ca2+] triggered through activation of a surface Ca2+ receptor. Closer analyses of the increases in cytosolic [Ca2+] associated with receptor activation are hindered by the action of this ion both as extracellular agonist and intracellular second messenger. Variations in the peak cytosolic [Ca2+] response to external Ca2+ with changes in cell membrane potential by K+ and valinomycin establish a contribution from extracellular Ca2+. Use of CIO4-, Ni2+ and Cd2+ as surrogate activators in low extracellular [Ca2+] indicate a contribution from Ca2+ release from intracellular stores as well. Such agonists also modify Ca2+ redistribution in other systems, such as skeletal muscle. Thus, we may gain insights into osteoclast extracellular Ca2+ detection and transduction from known features of more well-characterised cell systems.
Division of Biochemical Medicine, St George's Hospital Medical School, London, UK.
M
M
Zaidi
A S
AS
Alam
C L
CL
Huang
M
M
Pazianas
C M
CM
Bax
B E
BE
Bax
B S
BS
Moonga
P J
PJ
Bevis
V S
VS
Shankar
D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D005246:Feedback; D006801:Humans; D008564:Membrane Potentials; D010010:Osteoclasts / Q000187:drug effects / Q000502:physiology*
D015220:Calcium Channels; D002118:Calcium