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Titolo:
Coupling strength between localized Ca2+ transients and K+ channels is regulated by protein kinase C
Autore:
Bayguinov, O; Hagen, B; Kenyon, JL; Sanders, KM;
Indirizzi:
Univ Nevada, Sch Med, Dept Physiol & Cell Biol, Reno, NV 89557 USA Univ Nevada Reno NV USA 89557 ept Physiol & Cell Biol, Reno, NV 89557 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
fascicolo: 5, volume: 281, anno: 2001,
pagine: C1512 - C1523
SICI:
0363-6143(200111)281:5<C1512:CSBLCT>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE CELLS; ACTIVATED POTASSIUM CHANNELS; MURINE COLONIC MYOCYTES; CALCIUM-RELEASE; INOSITOL TRISPHOSPHATE; INTRACELLULAR CALCIUM; OUTWARD CURRENTS; SPARKS; TRANSLOCATION; CONTRACTION;
Keywords:
calcium puffs; spontaneous transient outward current; gastrointestinal motility; inositol 1,4,5-trisphosphate; sarcoplasmic reticulum;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Sanders, KM Univ Nevada, Sch Med, Dept Physiol & Cell Biol, MS 352, Reno, NV 89557 USA Univ Nevada MS 352 Reno NV USA 89557 S 352, Reno, NV 89557 USA
Citazione:
O. Bayguinov et al., "Coupling strength between localized Ca2+ transients and K+ channels is regulated by protein kinase C", AM J P-CELL, 281(5), 2001, pp. C1512-C1523

Abstract

Localized Ca2+ transients resulting from inositol trisphosphate (IP3)-dependent Ca2+ release couple to spontaneous transient outward currents (STOCs)in murine colonic myocytes. Confocal microscopy and whole cell patch-clamptechniques were used to investigate coupling between localized Ca2+ transients and STOCs. Colonic myocytes were loaded with fluo 3. Reduction in external Ca2+ ([ Ca2+](o)) reduced localized Ca2+ transients but increased STOCamplitude and frequency. Simultaneous recordings of Ca2+ transients and STOCs showed increased coupling strength between Ca2+ transients and STOCs when [Ca2+](o) was reduced. Gd3+ (10 muM) did not affect Ca2+ transients but increased STOC amplitude and frequency. Similarly, an inhibitor of Ca2+ influx, 1-2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl) propoxy]ethyl-1H-imidazole (SKF-96365), increased STOC amplitude and frequency. A protein kinase C (PKC) inhibitor, GF-109203X, also increased the amplitude and frequency of STOCs but had no effect on Ca2+ transients. Phorbol 12-myristate 13-acetate (1 muM) reduced STOC amplitude and frequency but did not affect Ca2+ transients. 4 alpha -Phorbol (1 muM) had no effect on STOCs or Ca2+ transients. Single channel studies indicated that large-conductance Ca2+-activated K+ (BK) channels were inhibited by a Ca2+-dependent PKC. In summary 1) Ca2+ release from IP3 receptor-operated stores activates Ca2+-activated K+ channels;2) Ca2+ influx through nonselective cation channels facilitates activationof PKC; and 3) PKC reduces the Ca2+ sensitivity of BK channels, reducing the coupling strength between localized Ca2+ transients and BK channels.

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Documento generato il 29/03/20 alle ore 18:14:12