PMID- 14607246
OWN - NLM
STAT- MEDLINE
DCOM- 20040105
LR  - 20190701
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 74
IP  - 2-3
DP  - 2003 Dec 5
TI  - Signaling of ATP receptors in glia-neuron interaction and pain.
PG  - 189-97
AB  - ATP causes the activation of p38 or ERK1/2, mitogen activated protein kinases 
      (MAPKs) resulting in the release of tumor necrosis factor-alpha (TNF) and 
      Interleukin-6 (IL-6) from microglia. We examined the effect of TNF and IL-6 on 
      the protection from PC12 cell death by serum deprivation. When PC12 cells were 
      incubated with serum-free medium for 32 hr, their viability decreased to 30 %. 
      IL-6 alone slightly protected the death of PC12 cells, whereas TNF alone did not 
      show any protective effect. In the meanwhile, when PC12 cells were pretreated 
      with TNF for 6 hr and then incubated with IL-6 under the condition of serum-free, 
      the viability of PC12 cells dramatically increased. TNF induced an increase of 
      IL-6 receptor (IL-6R) expression in PC12 cells at 4-6 hr. These data suggested 
      that 6 hr pretreatment with TNF increased IL-6R expression in PC12 cells, leading 
      to an enhancement of IL-6-induced neuroprotective action.To elucidate the role of 
      p38 in pathological pain, we investigated whether p38 is activated in the spinal 
      cord of the neuropathic pain model. In the rats displaying a marked allodynia, 
      the level of phospho-p38 was increased in the microglia of injury side in the 
      dorsal horn. Intraspinal administration of p38 inhibitor suppressed the 
      allodynia. These results demonstrate that neuropathic pain hypersensitivity 
      depends upon the activation of p38 signaling pathway in microglia in the dorsal 
      horn following peripheral nerve injury.
FAU - Inoue, Kazuhide
AU  - Inoue K
AD  - Division of Biosignaling, National Institute of Health Sciences, 1-18-1 Kamiyoga, 
      Setagaya, 158-8501, Tokyo, Japan. inoue@nihs.go.jp
FAU - Koizumi, Schuichi
AU  - Koizumi S
FAU - Tsuda, Makoto
AU  - Tsuda M
FAU - Shigemoto-Mogami, Yukari
AU  - Shigemoto-Mogami Y
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 (Cytokines)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Purinergic P2)
RN  - 0 (Tumor Necrosis Factor-alpha)
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  - Blotting, Western
MH  - Cell Death
MH  - Cytokines/metabolism/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - Genes, p53/genetics
MH  - Interleukin-6/biosynthesis/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors/physiology
MH  - Neuroglia/*physiology
MH  - Neurons/*physiology
MH  - PC12 Cells
MH  - Pain/*physiopathology
MH  - Peripheral Nervous System Diseases/pathology
MH  - Posterior Horn Cells/physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Purinergic P2/*physiology
MH  - Signal Transduction/*physiology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/pharmacology
MH  - p38 Mitogen-Activated Protein Kinases
EDAT- 2003/11/11 05:00
MHDA- 2004/01/06 05:00
CRDT- 2003/11/11 05:00
PHST- 2003/11/11 05:00 [pubmed]
PHST- 2004/01/06 05:00 [medline]
PHST- 2003/11/11 05:00 [entrez]
AID - S0024320503008245 [pii]
AID - 10.1016/j.lfs.2003.09.006 [doi]
PST - ppublish
SO  - Life Sci. 2003 Dec 5;74(2-3):189-97. doi: 10.1016/j.lfs.2003.09.006.