Intracellular calcium puffs in osteoclasts.

@article{Radding1999IntracellularCP,
  title={Intracellular calcium puffs in osteoclasts.},
  author={Wilson Radding and Sheldon E. Jordan and Raymond B. Hester and Harry C. Blair},
  journal={Experimental cell research},
  year={1999},
  volume={253 2},
  pages={
          689-96
        }
}
We studied intracellular calcium ([Ca(2+)](i)) in acid-secreting bone-attached osteoclasts, which produce a high-calcium acidic extracellular compartment. Acid secretion and [Ca(2+)](i) were followed using H(+)-restricted dyes and fura-2 or fluo-3. Whole cell calcium of acid-secreting osteoclasts was approximately 100 nM, similar to cells on inert substrate that do not secrete acid. However, measurements in restricted areas of the cell showed [Ca(2+)](i) transients to 500-1000 nM consistent… 
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References

SHOWING 1-10 OF 31 REFERENCES
Localized calcium signaling in multinucleated osteoclasts
TLDR
The data show that osteoclasts can have different [Ca2+]i activities in apparently equivalent cellular regions, no matter how generated, which suggests that there can be a number of spatially separate Ca2+ regulatory systems within an osteoclast cell body.
Extracellular protons acidify osteoclasts, reduce cytosolic calcium, and promote expression of cell-matrix attachment structures.
TLDR
Findings suggest that osteoclasts adherent to bone lack functional voltage-operated Ca2+ channels, and they reduced [Ca2+]i in response to protons via a membrane residing Ca-ATPase, and this leads to decrements in intracellular pH and calcium, and appears to promote cell-matrix attachment.
Calcium influx and release in isolated rat osteoclasts
TLDR
A refillable intracellular source of cytosolic Ca2+ that could function in osteoclastic regulation is demonstrated by a comparison of fura‐2 signals in response to application of theCa2+ ionophore, ionomycin, in Ca(2+)‐containing and inCa(2+‐free bathing solutions.
ATP induces an intracellular calcium pulse in osteoclasts.
  • H. Yu, J. Ferrier
  • Biology, Medicine
    Biochemical and biophysical research communications
  • 1993
TLDR
The ATP effect is repeatable with no change in bathing medium, implying that this signalling pathway has a mechanism for adaptation to progressively higher levels of ATP.
Calcium signal induced by mechanical perturbation of osteoclasts
TLDR
Measurements show that rabbit osteoclasts transduce a mechanical perturbation of the cell membrane into a [Ca2+]i signal via both a calcium influx and an internal calcium release.
Estimation of intracellular calcium activity in confluent monolayers of primary cultures of quail medullary bone osteoclasts
TLDR
The findings further support the idea that quail osteoclasts are able to acquire a Ca2+ sensor or 'receptor' and thus to respond to [Ca2+]o in a similar manner to mammalian osteoclast when they are removed from the bone microenvironment, but retain a refractoriness to CT under these conditions.
The effects of extracellular calcium and epinephrine on cytosolic-free calcium in single rat adipocytes.
TLDR
Digital imaging revealed that adipocytes demonstrate a high degree of intracellular spatial heterogeneity and intercellular variability in the magnitude of response to both calcium and epinephrine, which appears to be dependent upon extra-cellular calcium.
Calmodulin concentrated at the osteoclast ruffled border modulates acid secretion
TLDR
Calmodulin concentration and distribution is modified by bone attachment, and that osteoclastic acid secretion is calmodulin regulated.
Nuclear calcium signalling by individual cytoplasmic calcium puffs
TLDR
Using confocal imaging, the subcellular origin of Can signals in Fluo‐3‐loaded HeLa cells is investigated, and it seems that the elementary Ca release system is designed to facilitate nuclear Ca signalling.
Direct effect of calcium channel antagonists on osteoclast function: alterations in bone resorption and intracellular calcium concentrations.
TLDR
The data suggest that calcium channel antagonists may bind to the calcium channel of the osteoclast and lock it in an open state, leading to increased [Ca2+]i and decreased bone resorption.
...
1
2
3
4
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