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Titolo:
THE EFFECTS OF BRADYKININ ON K-15 CELLS TREATED WITH U73122, A PHOSPHOLIPASE-C INHIBITOR, OR NEOMYCIN( CURRENTS IN NG108)
Autore:
HILDEBRANDT JP; PLANT TD; MEVES H;
Indirizzi:
UNIV SAARLAND,INST PHYSIOL D-66421 HOMBURG GERMANY UNIV SAARLAND,INST PHYSIOL D-66421 HOMBURG GERMANY
Titolo Testata:
British Journal of Pharmacology
fascicolo: 5, volume: 120, anno: 1997,
pagine: 841 - 850
SICI:
0007-1188(1997)120:5<841:TEOBOK>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLIOMA HYBRID-CELLS; INOSITOL 1,4,5-TRISPHOSPHATE; CALCIUM MOBILIZATION; INTRACELLULAR CA-2+; CHANNELS; CA2+; PHOSPHOINOSITIDES; TRISPHOSPHATE; PLATELETS; RESPONSES;
Keywords:
U73122; NEOMYCIN; BRADYKININ; NG108-15 CELLS; M CURRENT; PHOSPHOLIPASE C;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
J.P. Hildebrandt et al., "THE EFFECTS OF BRADYKININ ON K-15 CELLS TREATED WITH U73122, A PHOSPHOLIPASE-C INHIBITOR, OR NEOMYCIN( CURRENTS IN NG108)", British Journal of Pharmacology, 120(5), 1997, pp. 841-850

Abstract

1 Bradykinin has multiple effects on differentiated NG108-15 neuroblastoma x glioma cells: it increases Ins(1,4,5)P-3 production and intracellular Ca2+ concentration [Ca2+](i), evokes a Ca2+ activated K+ current (I-K(Ca)) and inhibits M current (I-M). We studied the effect of the aminosteroid U73122 and the antibiotic neomycin, both putative blockers of phospholipase C (PLC), on these four bradykinin effects. 2 Preincubation with 1 or 5 mu M U73122 for 15 min partly suppressed Ins(1,4,5)P-3 generation and the increase in [Ca2+](i) induced by 1 mu M bradykinin. U73122 10 mu M caused total and irreversible inhibition. The inactive analogue U73343 was without effect. 3 Resting levels of Ins(1,4,5)P-3 were not affected. However, resting [Ca2+](i) was increased by10 mu M U73122, but not by U73343. Individual cells responded to 10 mu M U73122 With a small increase in [Ca2+](i), followed in some cells by a large further rise. 4 Pretreatment of whole-cell clamped cells with 1 mu M U73122 for 30 min reduced the bradykinin-induced I-K(Ca) to a fifth of its normal size. To suppress it totally, a 7-12 min pretreatment with 5 mu M U73122 was required. Again, U73343 was without effect. 5 U73122 and U73343 at concentrations of 5-10 mu M irreversibly decreased the holding current (I-h) which at a holding potential of -30 or -20 mV mainly flows through open M channels. The decrease was often preceded by a transient increase. 6 M current (I-M) measured with 1 s pulses, was also decreased by 5-10 mu M U73122 and U73343, but short applications of U73122 could cause a small increase. The bradykinin-induced inhibition of I-M was not affected by U73122. 7 Preincubation with 1 or 3 mM neomycin for 15 min did not affect Ins(1,4,5)P-3 generation and the increase in [Ca2+](i) induced by bradykinin. Pretreatment with 3 mM neomycin for about 20 min diminished the bradykinin-induced I-K(Ca) to a fifth of its normal size. 8 The four main conclusions drawnfrom the results are: (a) U73122 suppresses bradykinin-induced PLC activation and I-K(Ca), but not I-M inhibition. (b) This indicates that the transient outward current I-K(Ca), but not the decrease of I-M in response to bradykinin, is mediated by PLC. (c) U73122 itself inhibitsI-M and mobilizes Ca2+ from intracellular stores. (d) Externally applied neomycin is not an effective inhibitor of PLC-mediated signalling pathways in NG108-15 cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 02:54:40