PMID- 10899924
OWN - NLM
STAT- MEDLINE
DCOM- 20000817
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 75
IP  - 2
DP  - 2000 Aug
TI  - Brain-derived neurotrophic factor accelerates nitric oxide donor-induced 
      apoptosis of cultured cortical neurons.
PG  - 494-502
AB  - Brain-derived neurotrophic factor (BDNF) is known to have important functions in 
      neuronal survival, differentiation, and plasticity. In addition to its role as a 
      survival-promoting factor, BDNF reportedly can enhance neuronal cell death in 
      some cases, for example, the death caused by excitotoxicity or glucose 
      deprivation. The cellular mechanism of the death-enhancing effect of BDNF remains 
      unknown, in contrast to that of its survival-promoting effect. In this work, we 
      found that BDNF markedly accelerated the nitric oxide (NO) donor-induced death of 
      cultured embryonic cortical neurons. BDNF increased the number of cells with 
      nuclear condensation and DNA fragmentation 24 h after treatment with the NO 
      donor, but it did not change the number of those cells 36 h after the treatment. 
      The BDNF-accelerated death of cortical neurons was inhibited by the addition of 
      actinomycin D or cycloheximide. These results suggest that BDNF can accelerate 
      apoptotic cell death elicited by NO donor. TrkB-IgG and K252a blocked the 
      BDNF-induced acceleration of the death, indicating that the death-accelerating 
      effect by BDNF is mediated by TrkB. In addition, the BDNF-accelerated apoptosis 
      was inhibited by the addition of SB202190 and SB203580, specific inhibitors of 
      p38 mitogen-activated protein kinase (MAPK), and U0126, a specific inhibitor of 
      MAPK/ERK kinase 1, indicating that the activation of both p38 MAPK and ERK is 
      involved in the signaling cascade of the BDNF-accelerated, NO donor-induced 
      apoptosis.
FAU - Ishikawa, Y
AU  - Ishikawa Y
AD  - Division of Protein Biosynthesis, Institute for Protein Research, Osaka 
      University, Osaka, Japan.
FAU - Ikeuchi, T
AU  - Ikeuchi T
FAU - Hatanaka, H
AU  - Hatanaka H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Butadienes)
RN  - 0 (Carbazoles)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Indole Alkaloids)
RN  - 0 (Nitric Oxide Donors)
RN  - 0 (Nitriles)
RN  - 0 (Pyridines)
RN  - 0 (U 0126)
RN  - 169D1260KM (Nitroprusside)
RN  - 1CC1JFE158 (Dactinomycin)
RN  - 97161-97-2 (staurosporine aglycone)
RN  - 98600C0908 (Cycloheximide)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - OU13V1EYWQ (SB 203580)
RN  - PVX798P8GI (4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Butadienes/pharmacology
MH  - Carbazoles/pharmacology
MH  - Cell Nucleus/drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cerebral Cortex/*cytology
MH  - Cycloheximide/pharmacology
MH  - DNA Fragmentation/drug effects
MH  - Dactinomycin/pharmacology
MH  - Drug Synergism
MH  - Embryo, Mammalian
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Imidazoles/pharmacology
MH  - Immunoglobulin G/pharmacology
MH  - Indole Alkaloids
MH  - Kinetics
MH  - Male
MH  - Mitogen-Activated Protein Kinase 3
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors
MH  - Neurons/cytology/*drug effects/physiology
MH  - Nitric Oxide Donors/*pharmacology
MH  - Nitriles/pharmacology
MH  - Nitroprusside/*pharmacology
MH  - Pyridines/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, trkB/antagonists & inhibitors
MH  - Signal Transduction/drug effects/physiology
MH  - p38 Mitogen-Activated Protein Kinases
EDAT- 2000/07/19 11:00
MHDA- 2000/08/19 11:00
CRDT- 2000/07/19 11:00
PHST- 2000/07/19 11:00 [pubmed]
PHST- 2000/08/19 11:00 [medline]
PHST- 2000/07/19 11:00 [entrez]
AID - 10.1046/j.1471-4159.2000.0750494.x [doi]
PST - ppublish
SO  - J Neurochem. 2000 Aug;75(2):494-502. doi: 10.1046/j.1471-4159.2000.0750494.x.