PMID- 1569926
OWN - NLM
STAT- MEDLINE
DCOM- 19920526
LR  - 20131121
IS  - 0026-895X (Print)
IS  - 0026-895X (Linking)
VI  - 41
IP  - 4
DP  - 1992 Apr
TI  - Characterization of the neuropeptide Y-induced intracellular calcium release in 
      human erythroleukemic cells.
PG  - 767-71
AB  - Human erythroleukemic (HEL) cells, loaded with fura-2, respond to neuropeptide Y 
      (NPY) with a fast and transient increase in intracellular calcium. The Y1 
      receptor-specific agonist (Leu-31,Pro-34)-NPY is 4-fold more potent and the 
      carboxyl-terminal fragment NPY13-36 is 150-fold less potent than NPY. Thus, it is 
      concluded that the response is mediated through the activation of a Y1 type of 
      NPY receptor. HEL cells do not respond to a second addition of NPY but do respond 
      to a further addition of alpha-thrombin (alpha-T). However, in a calcium-free 
      medium, prior stimulation with NPY largely inhibits a subsequent response to 
      alpha-T. Moreover, prior stimulation with alpha-T in the absence of external 
      calcium completely prevents the response to the addition of NPY, indicating a 
      common effector pathway. The latter is further reinforced by using thapsigargin 
      (TG), which has been shown to deplete the Inositol 1,4,5-trisphosphate-dependent 
      calcium pool in other systems. HEL cells preincubated with TG in calcium-free 
      medium fail to respond to either NPY or alpha-T. Likewise, prior stimulation with 
      NPY or alpha-T in calcium-free medium significantly inhibits the response to TG. 
      Preincubation of cells with phorbol esters strongly inhibits the NPY-induced 
      release of intracellular Ca2+ in HEL cells, an effect that is partially prevented 
      by preincubation of the cells with H7, a protein kinase C inhibitor. However, 
      neither the homologous nor the apparent heterologous desensitization of the NPY 
      receptor can be prevented by H7. It is concluded that NPY releases intracellular 
      Ca2+ from an inositol 1,4,5-trisphosphate-sensitive calcium pool, which is 
      restored by external calcium, and that NPY receptor desensitization is protein 
      kinase C independent.
FAU - Daniels, A J
AU  - Daniels AJ
AD  - Division of Pharmacology, Wellcome Research Laboratories, Research Triangle Park, 
      North Carolina 27709.
FAU - Matthews, J E
AU  - Matthews JE
FAU - Humberto Viveros, O
AU  - Humberto Viveros O
FAU - Lazarowski, E R
AU  - Lazarowski ER
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Mol Pharmacol
JT  - Molecular pharmacology
JID - 0035623
RN  - 0 (Isoquinolines)
RN  - 0 (Neuropeptide Y)
RN  - 0 (Piperazines)
RN  - 0 (Terpenes)
RN  - 67526-95-8 (Thapsigargin)
RN  - 84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
MH  - Calcium/*metabolism
MH  - Enzyme Activation
MH  - Erythrocytes/metabolism
MH  - Fura-2
MH  - Humans
MH  - Inositol 1,4,5-Trisphosphate/metabolism
MH  - Isoquinolines/pharmacology
MH  - Leukemia, Erythroblastic, Acute
MH  - Neuropeptide Y/*physiology
MH  - Piperazines/pharmacology
MH  - Protein Kinase C/antagonists & inhibitors/metabolism
MH  - Spectrometry, Fluorescence
MH  - Terpenes/pharmacology
MH  - Thapsigargin
MH  - Tumor Cells, Cultured
EDAT- 1992/04/01 00:00
MHDA- 1992/04/01 00:01
CRDT- 1992/04/01 00:00
PHST- 1992/04/01 00:00 [pubmed]
PHST- 1992/04/01 00:01 [medline]
PHST- 1992/04/01 00:00 [entrez]
PST - ppublish
SO  - Mol Pharmacol. 1992 Apr;41(4):767-71.