PMID- 8978507
OWN - NLM
STAT- MEDLINE
DCOM- 19970317
LR  - 20190116
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 46
IP  - 6
DP  - 1996 Dec 15
TI  - Chemokine expression in rat stab wound brain injury.
PG  - 727-33
AB  - A traumatic injury to the adult mammalian central nervous system (CNS) results in 
      reactive astrogliosis and the migration of hematogenous cells into the damaged 
      neural tissue. Chemokines, a novel class of chemoattractant cytokines, are now 
      being recognized as mediators of the inflammatory changes that occur following 
      injury. The expression of MCP-1 (macrophage chemotactic peptide-1), a member of 
      the beta family of chemokines, has recently been demonstrated in trauma in the 
      rat brain (Berman et al.: J Immunol 156:3017-3023, 1996). Using a stab wound 
      model for mechanical injury, we studied the expression of two other beta 
      chemokines: RANTES (Regulated on Activation, Normal T cell Expressed and 
      Secreted) and MIP-1 beta (macrophage inflammatory protein-1 beta) in the rat 
      brain. The stab wound injury was characterized by widespread gliosis and 
      infiltration of hematogenous cells. Immunohistochemical staining revealed the 
      presence of RANTES and MIP-1 beta in the injured brain. RANTES and MIP-1 beta 
      were both diffusely expressed in the necrotic tissue and were detected as early 
      as 1 day post-injury (dpi). Double-labeling studies showed that MIP-1 beta, but 
      not RANTES, was expressed by reactive astrocytes near the lesion site. In 
      addition, MIP-1 beta staining was also detected on macrophages at the site of 
      injury. The initial expression of the chemokines closely correlated with the 
      appearance of inflammatory cells in the injured CNS, suggesting that RANTES and 
      MIP-1 beta may play a role in the inflammatory events of traumatic brain injury. 
      This study also demonstrates for the first time MIP-1 beta expression in reactive 
      astrocytes following trauma to the rat CNS.
FAU - Ghirnikar, R S
AU  - Ghirnikar RS
AD  - Department of Pathology, VAPA Health Care System, Palo Alto, CA 94304, USA.
FAU - Lee, Y L
AU  - Lee YL
FAU - He, T R
AU  - He TR
FAU - Eng, L F
AU  - Eng LF
LA  - eng
GR  - NS-11632/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokines)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Macrophage Inflammatory Proteins)
SB  - IM
MH  - Animals
MH  - Antibody Specificity
MH  - Astrocytes/chemistry/metabolism
MH  - Brain Chemistry/physiology
MH  - Brain Injuries/*metabolism/pathology/physiopathology
MH  - Chemokine CCL4
MH  - Chemokine CCL5/immunology/metabolism
MH  - Chemokines/*biosynthesis
MH  - Glial Fibrillary Acidic Protein/immunology/metabolism
MH  - Gliosis/metabolism
MH  - Immunohistochemistry
MH  - Macrophage Inflammatory Proteins/immunology/metabolism
MH  - Necrosis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Wounds, Stab/*metabolism/pathology/physiopathology
EDAT- 1996/12/15 00:00
MHDA- 2000/06/20 09:00
CRDT- 1996/12/15 00:00
PHST- 1996/12/15 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1996/12/15 00:00 [entrez]
AID - 10.1002/(SICI)1097-4547(19961215)46:6<727::AID-JNR9>3.0.CO;2-H [pii]
AID - 10.1002/(SICI)1097-4547(19961215)46:6<727::AID-JNR9>3.0.CO;2-H [doi]
PST - ppublish
SO  - J Neurosci Res. 1996 Dec 15;46(6):727-33. doi: 
      10.1002/(SICI)1097-4547(19961215)46:6<727::AID-JNR9>3.0.CO;2-H.