PMID- 14625085
OWN - NLM
STAT- MEDLINE
DCOM- 20040220
LR  - 20191210
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 119
IP  - 2
DP  - 2003 Nov 26
TI  - Comparison of inhibitory effects of brain-derived neurotrophic factor and 
      insulin-like growth factor on low potassium-induced apoptosis and activation of 
      p38 MAPK and c-Jun in cultured cerebellar granule neurons.
PG  - 184-91
AB  - On cell maturation following culture in medium containing 26 mM potassium (high 
      K+; HK), a change to medium containing 5 mM potassium (low K+; LK) rapidly 
      induces apoptosis in rat cerebellar granule neurons. Brain-derived neurotrophic 
      factor (BDNF) and insulin-like growth factor-1 (IGF-1) have survival-promoting 
      effects on the neurons via PI3-K. However, it remains unclear how they prevent 
      the apoptosis in the pathway downstream of phosphatidylinositol-3 kinase (PI3-K). 
      Recently, we have reported that PI3-K-ASK1 pathway is involved in 
      signal-transduction to p38 MAPK (p38)-c-Jun pathway. Here we found that IGF-1 had 
      a greater survival-promoting effect than BDNF, and activated PI3-K to a higher 
      level and maintained the level for a longer time. BDNF and IGF-1 suppressed the 
      activation of p38 and c-Jun, but not of c-Jun N-terminal kinase (JNK), caused by 
      lowering the potassium concentration. The inhibitory effects of IGF-1 were much 
      greater than those of BDNF. In addition, LY294002, a specific inhibitor of PI3-K, 
      cancelled the inhibitory effects of BDNF and IGF-1. These results suggest that 
      the greater inhibitory effects of IGF-1 than BDNF, on activation of p38 and c-Jun 
      and apoptosis, are caused by the higher level of PI3-K activation during 
      LK-induced apoptosis of cultured cerebellar granule neurons.
FAU - Yamagishi, Satoru
AU  - Yamagishi S
AD  - Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 
      565-0871, Japan. yamagishi@anat2.med.osaka-u.ac.jp
FAU - Matsumoto, Tomoya
AU  - Matsumoto T
FAU - Yokomaku, Daisaku
AU  - Yokomaku D
FAU - Hatanaka, Hiroshi
AU  - Hatanaka H
FAU - Shimoke, Koji
AU  - Shimoke K
FAU - Yamada, Masashi
AU  - Yamada M
FAU - Ikeuchi, Toshihiko
AU  - Ikeuchi T
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/drug effects/*physiology
MH  - Brain-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Cell Survival/drug effects/physiology
MH  - Cells, Cultured
MH  - Central Nervous System/cytology/enzymology/growth & development
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Insulin-Like Growth Factor I/*metabolism/pharmacology
MH  - JNK Mitogen-Activated Protein Kinases
MH  - Male
MH  - Mitogen-Activated Protein Kinases/drug effects/*metabolism
MH  - Neurons/drug effects/*enzymology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Phosphorylation/drug effects
MH  - Potassium Deficiency/enzymology
MH  - Proto-Oncogene Proteins c-jun/drug effects/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Signal Transduction/drug effects/physiology
MH  - p38 Mitogen-Activated Protein Kinases
EDAT- 2003/11/20 05:00
MHDA- 2004/02/21 05:00
CRDT- 2003/11/20 05:00
PHST- 2003/11/20 05:00 [pubmed]
PHST- 2004/02/21 05:00 [medline]
PHST- 2003/11/20 05:00 [entrez]
AID - S0169328X03004297 [pii]
AID - 10.1016/j.molbrainres.2003.09.009 [doi]
PST - ppublish
SO  - Brain Res Mol Brain Res. 2003 Nov 26;119(2):184-91. doi: 
      10.1016/j.molbrainres.2003.09.009.