Extracellular Calcium

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Edward M Brown - One of the best experts on this subject based on the ideXlab platform.

  • Extracellular Calcium sensing and signalling.
    Nature reviews. Molecular cell biology, 2003
    Co-Authors: Aldebaran M. Hofer, Edward M Brown
    Abstract:

    Ca2+ is well established as an intracellular second messenger. However, the molecular identification of a detector for Extracellular Ca2+ — the Extracellular Calcium-sensing receptor — has opened up the possibility that Ca2+ might also function as a messenger outside cells. Information about the local Extracellular Ca2+ concentration is conveyed to the interior of many cell types through this unique G-protein-coupled receptor. Here, we describe new emerging concepts concerning the signalling function of Extracellular Ca2+, with particular emphasis on the Extracellular Calcium-sensing receptor.

  • Expression of Extracellular Calcium-sensing receptor in human osteoblastic MG-63 cell line.
    American Journal of Physiology-cell Physiology, 2001
    Co-Authors: Toru Yamaguchi, Olga Kifor, Chianping Ye, Peter M. Vassilev, Jennifer L. Sanders, Naibedya Chattopadhyay, Edward M Brown
    Abstract:

    We have previously shown the expression of the Extracellular Calcium (Cao 2+)-sensing receptor (CaR) in osteoblast-like cell lines, and others have documented its expression in sections of murine, ...

  • Extracellular Calcium elicits a chemokinetic response from monocytes in vitro and in vivo
    The Journal of clinical investigation, 2000
    Co-Authors: Ivona T. Olszak, Edward M Brown, Mark C. Poznansky, Richard H. Evans, Douglas P. Olson, Claudine H. Kos, Martin R. Pollak, David T. Scadden
    Abstract:

    Recruitment of macrophages to sites of cell death is critical for induction of an immunologic response. Calcium concentrations in Extracellular fluids vary markedly, and are particularly high at sites of injury or infection. We hypothesized that Extracellular Calcium participates in modulating the immune response, perhaps acting via the seven-transmembrane Calcium-sensing receptor (CaR) on mature monocytes/macrophages. We observed a dose-dependent increase in monocyte chemotaxis in response to Extracellular Calcium or the selective allosteric CaR activator NPS R-467. In contrast, monocytes derived from mice deficient in CaR lacked the normal chemotactic response to a Calcium gradient. Notably, CaR activation of monocytes bearing the receptor synergistically augmented the transmigration response of monocytes to the chemokine MCP-1 in association with increased cell-surface expression of its cognate receptor, CCR2. Conversely, stimulation of monocytes with MCP-1 or SDF-1alpha reciprocally increased CaR expression, suggesting a dual-enhancing interaction of Ca(2+) with chemokines in recruiting inflammatory cells. Subcutaneous administration in mice of Ca(2+), MCP-1, or (more potently) the combination of Ca(2+) and MCP-1, elicited an inflammatory infiltrate consisting of monocytes/macrophages. Thus Extracellular Calcium functions as an ionic chemokinetic agent capable of modulating the innate immune response in vivo and in vitro by direct and indirect actions on monocytic cells. Calcium deposition may be both consequence and cause of chronic inflammatory changes at sites of injury, infection, and atherosclerosis.

  • Expression and Regulation by Extracellular Calcium in the AtT-20 Pituitary Cell Line
    1996
    Co-Authors: R L Emanuel, Gail K. Adler, O Kifor, K Krapcho, Steven Quinn, Forrest H. Fuller, Edward M Brown
    Abstract:

    A 120 kDa, G protein-coupled Calcium-sensing receptor (CaR) was recently identified and cloned from bovine parathyroid and rat kidney. We report here that a similar Calcium-sensing receptor is also present in rat and mouse pituitary as well as in the mouse pituitary cell line, AtT-20. Fragments (333-bp) of the Extracellular domain of the Calcium-sensing receptor from the AtT-20 cells and mouse pituitary were amplified by FIT-PCR, sequenced, and found to be identical. By Northern blot analysis, AtT-20 cells expressed a major CaR mRNA transcript of 7.5 kb and three minor transcripts of 9.5, 4.0, and 1.5 kb. Except for the 9.5-kb species, these CaR transcripts were also found to be present in mouse kidney, where the 7.5-kb transcript was again the predominant form. The presence of the CaR protein in AtT-20 cells was documented directly by fluorescence immunocytochemistry using an antibody directed against the Extracellular domain of the CaR. Exposure of AtT-20 cells to increasing Extracellular Calcium concentrations from 0.3 to 3 mM for 24 h resulted in a 2- to 4-fold increase in the levels of CaR mRNA, but not of the RNAs for p-actin or POMC. The CaR appeared to be functional in AtT-20 cells, since acute increases in Extracellular Calcium between 2 and 5 mM induced increases in the cellular content of total inositol phosphates, cytosolic Calcium, and CAMP. This report suggests that pituitary cells respond to changes in Extracellular Calcium via a G protein-coupled CaR. (Molecular Endocrinology 10: -3 1996)

  • Serpentine receptors for parathyroid hormone, calcitonin and Extracellular Calcium ions.
    Bailliere's clinical endocrinology and metabolism, 1996
    Co-Authors: Edward M Brown, Gino V. Segre, Steven R. Goldring
    Abstract:

    Summary The cloning of the receptors for PTH, CT and Extracellular Calcium ions represents a significant advance in the elucidation of the mechanisms through which Extracellular Calcium ions are regulated. All are members of the superfamily of GPCR, and the inclusion of the Ca 2+ o -sensing receptor in this superfamily documents that Extracellular Calcium ions can serve as an Extracellular first messenger, in addition to subserving their better known role as a key intracellular second messenger. Furthermore, it has proved possible to identify several human diseases that result from inactivating or activating mutations in the PTH or Ca 2+ o -sensing receptor. Finally, the availability of these cloned receptors will enable many more studies on structure—function relationships for these receptors as well as clarifying their tissue distribution, regulation and roles in health and disease. It may also be possible to design novel therapeutic agents that permit manipulation of the receptors when their function is abnormal.

Baofeng Yang - One of the best experts on this subject based on the ideXlab platform.

Qiu-shi Wang - One of the best experts on this subject based on the ideXlab platform.

Nicole Morel - One of the best experts on this subject based on the ideXlab platform.

  • Extracellular Calcium modulates the inhibitory effect of 4-aminopyridine on Kv current in vascular smooth muscle cells.
    European Journal of Pharmacology, 2013
    Co-Authors: Nicolas Baeyens, V A Bouryi, Nicole Morel
    Abstract:

    4-Aminopyridine is widely used as a Kv channel blocker. However, its mechanism of action is still a matter of debate. Extracellular Calcium as well as 4-aminopyridine have been reported to interact with the activation kinetics of particular Kv channels. The objective of the present study was to investigate whether Extracellular Calcium could modulate the inhibition of Kv current by 4-aminopyridine in vascular myocytes. Kv current was recorded by using whole-cell patch-clamp in freshly isolated smooth muscle cells from rat mesenteric artery. Macroscopic properties of Kv current were not affected by change in Extracellular Calcium from 0 to 2 mM. During a 10 s depolarizing pulse, 4-aminopyridine inhibited the peak current without affecting the end-pulse current. The concentration-effect curve of 4-aminopyridine was shifted to the left in the presence of 2 mM Calcium compared to 0 Calcium. After 4-aminopyridine washout, current recovery from block was slower in the presence than in the absence of Calcium. Inhibition of Kv current by 4-aminopyridine (0.5 mM) and the Kv2 blocker stromatoxin (50 nM) was additive and stromatoxin did not alter the potentiation of 4-aminopyridine effect by Extracellular Calcium. These results showed that Extracellular Calcium modulated the inhibitory potency of 4-aminopyridine on Kv current in vascular myocytes. The component of Kv current that was inhibited by 4-aminopyridine in a Calcium-sensitive manner was distinct from Kv2 current. © 2013 Published by Elsevier B.V.

Wenjing Xing - One of the best experts on this subject based on the ideXlab platform.

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