PMID- 14552870
OWN - NLM
STAT- MEDLINE
DCOM- 20031031
LR  - 20190722
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 183
IP  - 2
DP  - 2003 Oct
TI  - Expression of the type 1 and type 2 receptors for tumor necrosis factor after 
      traumatic spinal cord injury in adult rats.
PG  - 286-97
AB  - Posttraumatic inflammation has been implicated in secondary tissue damage after 
      spinal cord injury (SCI). Tumor necrosis factor-alpha (TNF-alpha) is a key 
      inflammatory mediator that is increasingly expressed after SCI. The effect of 
      TNF-alpha is mediated through its receptors TNFR1 (p55) and TNFR2 (p75). However, 
      whether these two receptors are expressed after SCI has not been demonstrated. In 
      the present study, the temporo-spatial expression of TNFR1 and TNFR2 was examined 
      in rats that had received a 10 g impact injury dropped at a height of 12.5 mm 
      using the New York University impact device. In sham operates, no detectable 
      TNFR1 or TNFR2 immunoreactivity (IR) was observed. In contused spinal cord, TNFR1 
      protein expression and immunoreactivity (IR) were detected as early as 15 min 
      postinjury, reached its peak at 8 h, and declined markedly after 1 and 3 days 
      postinjury. The temporal pattern of TNFR2 expression was similar to that of TNFR1 
      but its expression peaked at 4 h postinjury. During peak expression, TNFR1- and 
      TNFR2-IR were most intense at the site of injury and decreased gradually from the 
      injury epicenter. TNFR1- and TNFR2-positive cells included neurons, astrocytes, 
      and oligodendrocytes. Methylprednisolone (MP), a synthetic glucocorticoid, 
      partially inhibited the injury-induced expression of TNFR1 and TNFR2, an effect 
      which could be reversed by RU486, an antagonist of glucocorticoid receptors. We 
      suggest that the expression of TNFR1 and TNFR2 after SCI may contribute to 
      posttraumatic inflammatory responses of TNF-alpha.
FAU - Yan, Ping
AU  - Yan P
AD  - Department of Anatomy and Neurobiology, Saint Louis University School of 
      Medicine, St. Louis, MO 63104, USA.
FAU - Liu, Naikui
AU  - Liu N
FAU - Kim, Gyeong-Moon
AU  - Kim GM
FAU - Xu, Jingming
AU  - Xu J
FAU - Xu, Jian
AU  - Xu J
FAU - Li, Qun
AU  - Li Q
FAU - Hsu, Chung Y
AU  - Hsu CY
FAU - Xu, Xiao-Ming
AU  - Xu XM
LA  - eng
GR  - NS36350/NS/NINDS NIH HHS/United States
GR  - NS37230/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Antigens, CD)
RN  - 0 (Hormone Antagonists)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 320T6RNW1F (Mifepristone)
RN  - X4W7ZR7023 (Methylprednisolone)
SB  - IM
MH  - Animals
MH  - Antigens, CD/*biosynthesis
MH  - Blotting, Western
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Female
MH  - Hormone Antagonists/pharmacology
MH  - Methylprednisolone/pharmacology
MH  - Mifepristone/pharmacology
MH  - Neuroprotective Agents/pharmacology
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptors, Tumor Necrosis Factor/*biosynthesis
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - Spinal Cord/drug effects/metabolism/pathology
MH  - Spinal Cord Injuries/drug therapy/*metabolism/pathology
EDAT- 2003/10/14 05:00
MHDA- 2003/11/01 05:00
CRDT- 2003/10/14 05:00
PHST- 2003/10/14 05:00 [pubmed]
PHST- 2003/11/01 05:00 [medline]
PHST- 2003/10/14 05:00 [entrez]
AID - S0014488603001353 [pii]
AID - 10.1016/s0014-4886(03)00135-3 [doi]
PST - ppublish
SO  - Exp Neurol. 2003 Oct;183(2):286-97. doi: 10.1016/s0014-4886(03)00135-3.