INHIBITION OF BRADYKININ-INDUCED CYTOSOLIC CA2+ ELEVATION BY MUSCARINIC STIMULATION WITHOUT ATTENUATION OF INOSITOL 1,4,5-TRISPHOSPHATE PRODUCTION IN HUMAN NEUROBLASTOMA SK-N-BE(2)C CELLS
SCIE
SCOPUS
- Title
- INHIBITION OF BRADYKININ-INDUCED CYTOSOLIC CA2+ ELEVATION BY MUSCARINIC STIMULATION WITHOUT ATTENUATION OF INOSITOL 1,4,5-TRISPHOSPHATE PRODUCTION IN HUMAN NEUROBLASTOMA SK-N-BE(2)C CELLS
- Authors
- SUH, BC; KIM, KT
- Date Issued
- 1995-11
- Publisher
- LIPPINCOTT-RAVEN PUBL
- Abstract
- Cross talk between two phospholipase C (PLC)-linked receptor signalings was investigated in SK-N-BE(2)C human neuroblastoma cells. Sequential stimulation with two agonists at 5-min intervals was performed to examine the interaction between muscarinic and bradykinin (BK) receptors. Pretreatment of cells with a maximal effective concentration (5 mu M) of BK did not affect the subsequent carbachol (CCh)-induced [Ca2+](i) rise, but CCh (1 mM) pretreatment completely abolished the BK-induced [Ca2+](i) rise without inhibition of BK-induced inositol 1,4,5-trisphosphate (IP3) generation. Thapsigargin (1 mu M) pretreatment abolished the subsequent BK- and CCh-induced [Ca2+](i) rise, though it did not affect agonist-induced IP3 generation. However, the addition of atropine at plateau phases of CCh-induced [Ca2+](i) rise and IP3 production caused a rapid decline to the basal levels and then restored the [Ca2+](i) rise by BK. Treatment of cells with both CCh and BK at the same time showed additive effects in IP3 production. However, the [Ca2+](i) rise induced by both agonists in the presence or absence of extracellular Ca2+ was the same as the responses triggered by CCh alone. The results suggest that each receptor or receptor-linked PLC activity is not influenced by pretreatment with the other agonist but IP3-sensitive Ca2+ stores are shared by signal pathways from both receptors.
- Keywords
- CARBACHOL; BRADYKININ; PHOSPHOLIPASE C; INTRACELLULAR CA2+; INOSITOL 1,4,5-TRISPHOSPHATE; SK-N-BE(2)C NEUROBLASTOMA; NEURO-BLASTOMA CELLS; PROTEIN-KINASE-C; RECEPTOR; ACTIVATION; INFLUX; STORES; 1,3,4,5-TETRAKISPHOSPHATE; EXPRESSION; MESSENGER; CALCIUM
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/21708
- DOI
- 10.1046/j.1471-4159.1995.65052124.x
- ISSN
- 0022-3042
- Article Type
- Article
- Citation
- JOURNAL OF NEUROCHEMISTRY, vol. 65, no. 5, page. 2124 - 2130, 1995-11
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- There are no files associated with this item.
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