scholarly journals cAMP regulates nitric oxide production and ouabain sensitive Na + , K + -ATPase activity in SH-SY5Y human neuroblastoma cells

Diabetologia ◽  
1998 ◽  
Vol 41 (12) ◽  
pp. 1451-1458 ◽  
Author(s):  
H. Inada ◽  
H. Shindo ◽  
M. Tawata ◽  
T. Onaya
Keyword(s):  
Nitric Oxide ◽  
Atpase Activity ◽  
Neuroblastoma Cells ◽  
Nitric Oxide Production ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Oxide Production

scholarly journals Adrenomedullin Stimulates Nitric Oxide Release from SK-N-SH Human Neuroblastoma Cells by Modulating Intracellular Calcium Mobilization

Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2295-2305 ◽  
Author(s):  
Yong Xu ◽  
Teresa L. Krukoff
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Intracellular Calcium ◽  
Protein Kinase A ◽  
Neuroblastoma Cells ◽  
No Synthase ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
No Release ◽  
Kinase A

Abstract We used SK-N-SH human neuroblastoma cells to test the hypothesis that adrenomedullin (ADM), a multifunctional neuropeptide, stimulates nitric oxide (NO) release by modulating intracellular free calcium concentration ([Ca2+]i) in neuron-like cells. We used a nitrite assay to demonstrate that ADM (10 pm to 100 nm) stimulated NO release from the cells, with a maximal response observed with 1 nm at 30 min. This response was blocked by 1 nm ADM22–52, an ADM receptor antagonist or 2 μm vinyl-l-NIO, a neuronal NO synthase inhibitor. In addition, 5 μm 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester, an intracellular calcium chelator, eliminated the ADM-induced NO release. Similar results were observed when the cells were incubated in calcium-free medium or when l-type calcium channels were inhibited with 5 μm nifedipine or 10 μm nitrendipine. Depletion of calcium stores in the endoplasmic reticulum (ER) with 1 μm cyclopiazonic acid or 150 nm thapsigargin, or inhibition of ryanodine-sensitive receptors in the ER with 10 μm ryanodine attenuated the ADM-induced NO release. NO responses to ADM were mimicked by 1 mm dibutyryl cAMP, a cAMP analog, and were abrogated by 5 μm H-89, a protein kinase A inhibitor. Furthermore, Fluo-4 fluorescence-activated cell sorter analysis showed that ADM (1 nm) significantly increased [Ca2+]i at 30 min. This response was blocked by nifedipine (5 μm) or H-89 (5 μm) and was reduced by ryanodine (10 μm). These results suggest that ADM stimulates calcium influx through l-type calcium channels and ryanodine-sensitive calcium release from the ER, probably via cAMP-protein kinase A-dependent mechanisms. These elevations in [Ca2+]i cause activation of neuronal NO synthase and NO release.

scholarly journals Antiproliferative effect of nitric oxide on epidermal growth factor-responsive human neuroblastoma cells

2002 ◽  
Vol 83 (1) ◽  
pp. 119-131 ◽  
Author(s):  
Maribel Murillo-Carretero ◽  
María José Ruano ◽  
Esperanza R. Matarredona ◽  
Antonio Villalobo ◽  
Carmen Estrada
Keyword(s):  
Nitric Oxide ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Neuroblastoma Cells ◽  
Antiproliferative Effect ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Epidermal Growth

scholarly journals Nitric oxide prevents H2O2-induced apoptosis in SK-N-MC human neuroblastoma cells

2018 ◽  
Vol 14 (14) ◽  
pp. 1974-1984 ◽  
Author(s):  
Yeong-Min Yoo ◽  
Eui-Man Jung ◽  
Changhwan Ahn ◽  
Eui-Bae Jeung
Keyword(s):  
Nitric Oxide ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Induced Apoptosis
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