PMID- 9751191
OWN - NLM
STAT- MEDLINE
DCOM- 19981014
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 71
IP  - 4
DP  - 1998 Oct
TI  - Cellular localization and temporal elevation of tumor necrosis factor-alpha, 
      interleukin-1 alpha, and transforming growth factor-beta 1 mRNA in hippocampal 
      injury response induced by trimethyltin.
PG  - 1577-87
AB  - In certain pathologic states, cytokine production may become spatially and 
      temporally dysregulated, leading to their inappropriate production and 
      potentially detrimental consequences. Tumor necrosis factor-alpha (TNF-alpha), 
      interleukin (IL)-1, IL-6, and transforming growth factor-beta (TGF-beta) mediate 
      a range of host responses affecting multiple cell types. To study the role of 
      cytokines in the early stages of brain injury, we examined alterations in the 
      17-day-old mouse hippocampus during trimethyltin-induced neurodegeneration 
      characterized by neuronal necrosis, microglia activation in the dentate, and 
      astrocyte reactivity throughout the hippocampus. By 24 h after dosing, elevations 
      in mRNA levels for TNF-alpha, IL-1alpha, IL-1beta, and IL-6 mRNA were seen. 
      TGF-beta1 mRNA was elevated at 72 h. In situ hybridization showed that TNF-alpha 
      and IL-1alpha were localized to the microglia, whereas TGF-beta1 was expressed 
      predominantly in hippocampal pyramidal cells. Intercellular adhesion molecule-1, 
      EB-22, Mac-1, and glial fibrillary acidic protein mRNA levels were elevated 
      within the first 3 days of exposure in the absence of increased inducible nitric 
      oxide synthetase and interferon-gamma mRNA. These data suggest that 
      pro-inflammatory cytokines contribute to the progression and pattern of neuronal 
      degeneration in the hippocampus.
FAU - Bruccoleri, A
AU  - Bruccoleri A
AD  - Laboratory of Neurotoxicology, National Institute of Environmental Health 
      Sciences, National Institutes of Health, Research Triangle Park, North Carolina 
      17709, USA.
FAU - Brown, H
AU  - Brown H
FAU - Harry, G J
AU  - Harry GJ
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Synaptophysin)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Trimethyltin Compounds)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1631-73-8 (trimethyltin)
RN  - EC 3.1.- (Ribonucleases)
SB  - IM
MH  - Animals
MH  - Hippocampus/drug effects/*metabolism/pathology
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Interleukin-1/genetics/*metabolism
MH  - Male
MH  - Mice
MH  - RNA, Messenger/*metabolism
MH  - Ribonucleases/metabolism
MH  - Synaptophysin/analysis
MH  - Time Factors
MH  - Transforming Growth Factor beta/genetics/*metabolism
MH  - Trimethyltin Compounds/*toxicity
MH  - Tumor Necrosis Factor-alpha/genetics/*metabolism
EDAT- 1998/09/29 00:00
MHDA- 1998/09/29 00:01
CRDT- 1998/09/29 00:00
PHST- 1998/09/29 00:00 [pubmed]
PHST- 1998/09/29 00:01 [medline]
PHST- 1998/09/29 00:00 [entrez]
AID - 10.1046/j.1471-4159.1998.71041577.x [doi]
PST - ppublish
SO  - J Neurochem. 1998 Oct;71(4):1577-87. doi: 10.1046/j.1471-4159.1998.71041577.x.