PMID- 16267827
OWN - NLM
STAT- MEDLINE
DCOM- 20060428
LR  - 20161124
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 82
IP  - 5
DP  - 2005 Dec 1
TI  - Differential role of tumor necrosis factor receptors in mouse brain inflammatory 
      responses in cryolesion brain injury.
PG  - 701-16
AB  - Tumor necrosis factor-alpha (TNF-alpha) is one of the mediators dramatically 
      increased after traumatic brain injury that leads to the activation, 
      proliferation, and hypertrophy of mononuclear, phagocytic cells and gliosis. 
      Eventually, TNF-alpha can induce both apoptosis and necrosis via intracellular 
      signaling. This cytokine exerts its functions via interaction with two receptors: 
      type-1 receptor (TNFR1) and type-2 receptor (TNFR2). In this work, the 
      inflammatory response after a freeze injury (cryolesion) in the cortex was 
      studied in wild-type (WT) animals and in mice lacking TNFR1 (TNFR1 KO) or TNFR2 
      (TNFR2 KO). Lack of TNFR1, but not of TNFR2, significantly decreased the 
      inflammatory response and tissue damage elicited by the cryolesion at both 3 and 
      7 days postlesion, with decreased gliosis, lower IL-1beta immunostaining, and a 
      reduction of apoptosis markers. Cryolesion produced a clear induction of the 
      proinflammatory cytokines interleukin (IL)-1alpha, IL-1beta, IL-6, and TNF-alpha; 
      this induction was significantly lower in the TNFR1 KO mice. Host response genes 
      (ICAM-1, A20, EB22/5, and GFAP) were also induced by the cryolesion, but to a 
      lesser extent in TNFR1 KO mice. Lack of TNFR1 signaling also affected the 
      expression of apoptosis/cell death-related genes (Fas, Rip, p53), matrix 
      metalloproteinases (MMP3, MMP9, MMP12), and their inhibitors (TIMP1), suggesting 
      a role of TNFR1 in extracellular matrix remodeling after injury. However, GDNF, 
      NGF, and BDNF expression were not affected by TNFR1 deficiency. Overall, these 
      results suggest that TNFR1 is involved in the early establishment of the 
      inflammatory response and that its deficiency causes a decreased inflammatory 
      response and tissue damage following brain injury.
FAU - Quintana, Albert
AU  - Quintana A
AD  - Institute of Neurosciences and Department of Cellular Biology, Physiology and 
      Immunology, Animal Physiology Unit, Faculty of Sciences, Autonomous University of 
      Barcelona, Bellaterra, Barcelona, Spain.
FAU - Giralt, Mercedes
AU  - Giralt M
FAU - Rojas, Santiago
AU  - Rojas S
FAU - Penkowa, Milena
AU  - Penkowa M
FAU - Campbell, Iain L
AU  - Campbell IL
FAU - Hidalgo, Juan
AU  - Hidalgo J
FAU - Molinero, Amalia
AU  - Molinero A
LA  - eng
GR  - MH62231/MH/NIMH NIH HHS/United States
GR  - NS36979/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Cytokines)
RN  - 0 (Growth Substances)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor Decoy Receptors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1IEO802L3J (recombinant human tumor necrosis factor-binding protein-1)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Brain/*metabolism/physiopathology
MH  - Brain Injuries/genetics/*metabolism/physiopathology
MH  - Cold Temperature/adverse effects
MH  - Cytokines/metabolism
MH  - Denervation
MH  - Disease Models, Animal
MH  - Down-Regulation/physiology
MH  - Encephalitis/genetics/*metabolism/physiopathology
MH  - Female
MH  - Gene Expression Regulation/genetics
MH  - Genes, Immediate-Early/physiology
MH  - Gliosis/genetics/metabolism/physiopathology
MH  - Growth Substances/genetics
MH  - Mice
MH  - Mice, Knockout
MH  - Nerve Degeneration/genetics/*metabolism/physiopathology
MH  - Receptors, Tumor Necrosis Factor/*genetics
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II/genetics
MH  - Tumor Necrosis Factor Decoy Receptors
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2005/11/04 09:00
MHDA- 2006/04/29 09:00
CRDT- 2005/11/04 09:00
PHST- 2005/11/04 09:00 [pubmed]
PHST- 2006/04/29 09:00 [medline]
PHST- 2005/11/04 09:00 [entrez]
AID - 10.1002/jnr.20680 [doi]
PST - ppublish
SO  - J Neurosci Res. 2005 Dec 1;82(5):701-16. doi: 10.1002/jnr.20680.