PMID- 10954053
OWN - NLM
STAT- MEDLINE
DCOM- 20000831
LR  - 20190701
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 67
IP  - 10
DP  - 2000
TI  - Anti-apoptotic action of nerve growth factor in mouse osteoblastic cell line.
PG  - 1197-206
AB  - We investigated the potential role of nerve growth factor (NGF) in osteoblast 
      survival in vitro. We found the expression of the mRNAs encoding NGF, 
      brain-derived neurotrophic factor (BDNF), and trk-b, which is the receptor 
      molecule of BDNF in mouse osteoblastic MC3T3-E1 cells. NGF high-affinity receptor 
      trk-a was expressed continuously in the cells as visualized by Western blotting. 
      A proinflammatory cytokine mixture stimulated NGF mRNA, and NGF protein release 
      from MC3T3-E1 cells. When the effect of the nuclear factor-KB inhibitor 
      pyrrolidine dithiocarbamate (PDTC) and activating protein-1 inhibitor curcumin 
      were examined, a dose-dependent inhibition of cytokine-activated NGF expression 
      occurred in the presence of PDTC or curcumin. Further, a specific inhibitor of 
      p38 mitogen activated protein kinase (MAPK), i.e., SB203580, inhibited the 
      induction of NGF in cytokines-treated cells in a dose-dependent manner whereas a 
      specific inhibitor of classic MAPK, PD98059 had no effect on the induction of 
      NGF. Treatment of anti-NGF IgG resulted in a potent increase of DNA fragmentation 
      at a dose-dependent manner. NGF but not BDNF caused a dose-dependent reduction in 
      the extent of apoptotic DNA breakdown under treatment with cytokines. Under 
      similar conditions, the addition of NGF resulted in a potent reduction in bax 
      protein but not in Fas, or bcl-xl. These findings demonstrated that NGF in 
      non-neuronal osteoblastic cells may play an important role in cell survival as an 
      anti-apoptotic factor.
FAU - Mogi, M
AU  - Mogi M
AD  - Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya, 
      Japan.
FAU - Kondo, A
AU  - Kondo A
FAU - Kinpara, K
AU  - Kinpara K
FAU - Togari, A
AU  - Togari A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cytokines)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Flavonoids)
RN  - 0 (Imidazoles)
RN  - 0 (NF-kappa B)
RN  - 0 (Pyridines)
RN  - 0 (Pyrrolidines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiocarbamates)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - OU13V1EYWQ (SB 203580)
RN  - SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/genetics
MH  - Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors
MH  - Cytokines/pharmacology
MH  - DNA Fragmentation/drug effects
MH  - Enzyme Inhibitors/pharmacology
MH  - Flavonoids/pharmacology
MH  - Humans
MH  - Imidazoles/pharmacology
MH  - MAP Kinase Signaling System/drug effects/physiology
MH  - Mice
MH  - NF-kappa B/antagonists & inhibitors/physiology
MH  - Nerve Growth Factor/biosynthesis/genetics/*physiology
MH  - Osteoblasts/*cytology/drug effects/metabolism
MH  - Pyridines/pharmacology
MH  - Pyrrolidines/pharmacology
MH  - RNA, Messenger/biosynthesis/genetics/metabolism
MH  - Receptor, trkA/biosynthesis
MH  - Receptor, trkB/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Thiocarbamates/pharmacology
EDAT- 2000/08/23 11:00
MHDA- 2000/09/02 11:01
CRDT- 2000/08/23 11:00
PHST- 2000/08/23 11:00 [pubmed]
PHST- 2000/09/02 11:01 [medline]
PHST- 2000/08/23 11:00 [entrez]
AID - S0024320500007050 [pii]
AID - 10.1016/s0024-3205(00)00705-0 [doi]
PST - ppublish
SO  - Life Sci. 2000;67(10):1197-206. doi: 10.1016/s0024-3205(00)00705-0.