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Titolo:
Fundamental Ca2+ signaling mechanisms in mouse dendritic cells: CRAC is the major Ca2+ entry pathway
Autore:
Hsu, SF; OConnell, PJ; Klyachko, VA; Badminton, MN; Thomson, AW; Jackson, MB; Clapham, DE; Ahern, GP;
Indirizzi:
Harvard Univ, Childrens Hosp, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 rd Hughes Med Inst, Boston, MA 02115 USA Univ Pittsburgh, Med Ctr, TE Starzl Transplantat Inst, Pittsburgh, PA 15213 USA Univ Pittsburgh Pittsburgh PA USA 15213 at Inst, Pittsburgh, PA 15213 USA Univ Pittsburgh, Med Ctr, Dept Surg, Pittsburgh, PA 15213 USA Univ Pittsburgh Pittsburgh PA USA 15213 pt Surg, Pittsburgh, PA 15213 USA Univ Wisconsin, Dept Physiol, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 , Dept Physiol, Madison, WI 53706 USA Univ Wisconsin, Biophys Program, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 iophys Program, Madison, WI 53706 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 10, volume: 166, anno: 2001,
pagine: 6126 - 6133
SICI:
0022-1767(20010515)166:10<6126:FCSMIM>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPIDERMAL LANGERHANS CELLS; RAT MAST-CELLS; CALCIUM CHANNELS; PURINERGIC RECEPTOR; EXTRACELLULAR ATP; P2Y RECEPTORS; T-LYMPHOCYTES; MACROPHAGES; CHEMOKINES; DEPLETION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Ahern, GP So Illinois Univ, Dept Pharmacol, 801 N Rutledge, Springfield, IL 62702 USA So Illinois Univ 801 N Rutledge Springfield IL USA 62702 702 USA
Citazione:
S.F. Hsu et al., "Fundamental Ca2+ signaling mechanisms in mouse dendritic cells: CRAC is the major Ca2+ entry pathway", J IMMUNOL, 166(10), 2001, pp. 6126-6133

Abstract

Although Ca2+-signaling processes are thought to underlie many dendritic cell (DC) functions, the Ca2+ entry pathway's are unknown. Therefore, we investigated Ca2+-signaling in mouse myeloid DC using Ca2+ imaging and electrophysiological techniques. Neither Ca2+ currents nor changes in intracellular Ca2+ were detected following membrane depolarization, ruling out the presence of functional voltage-dependent Ca2+ channels. ATP, a purinergic receptor ligand, and 1-4 dihydropyridines, previously suggested to activate a plasma membrane Ca2+ channel in human myeloid DC, both elicited Ca2+ rises inmurine DC. However, in this study these responses were found to be due to mobilization from intracellular stores rather than by Ca2+ entry. In contrast, Ca2+ influx was activated by depletion of intracellular Ca2+ stores with thapsigargin, or inositol trisphosphate. This Ca2+ influx was enhanced bymembrane hyperpolarization, inhibited by SKIT 96365, and exhibited a cation permeability similar to the Ca2+ release-activated Ca2+ channel (CRAG) found in T lymphocytes. Furthermore, ATP, a putative DC chemotactic and maturation factor, induced a delayed Ca2+ entry with a voltage dependence similar to CRAC. Moreover, the level of phenotypic DC maturation was correlated with the extracellular Ca2+ concentration and enhanced by thapsigargin treatment. These results suggest that CRAC is a major pathway for Ca2+ entry in mouse myeloid DC and support the proposal that CRAC participates in DC maturation and migration.

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Documento generato il 07/08/20 alle ore 00:24:35