PMID- 8666808
OWN - NLM
STAT- MEDLINE
DCOM- 19960808
LR  - 20071114
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 156
IP  - 11
DP  - 1996 Jun 1
TI  - Chemokine monocyte chemoattractant protein-1 is expressed by astrocytes after 
      mechanical injury to the brain.
PG  - 4363-8
AB  - By 24 h after mechanical trauma to the cerebral cortex, astroglial reaction 
      begins and injury sites are infiltrated by activated mononuclear phagocytes 
      derived from blood-borne monocytes and endogenous microglia. There is little 
      information about cellular interactions between astrocytes and leukocytes during 
      this process. We previously showed that murine astrocytes produce chemokines 
      including monocyte chemoattractant protein-1 (MCP-1) during experimental 
      autoimmune encephalomyelitis. In this study, we asked whether astrocytes produce 
      MCP-1 in the absence of immune mediated inflammation. To address this question, 
      we analyzed the time course and cellular source of MCP-1 in mouse brain after 
      penetrating mechanical injury, with particular focus on early time points before 
      histologic detection of infiltrating mononuclear phagocytes. We observed sharply 
      increased steady state levels of MCP-1 mRNA within 3 h after nitrocellulose 
      membrane stab or implant injury to the adult mouse brain, and MCP-1 protein 
      elevations were documented at 12 h postinjury. In situ hybridization combined 
      with immunohistochemistry for the glial fibrillary acidic protein astrocyte 
      marker showed that astrocytes were the cellular source of MCP-1 mRNA at these 
      early time points after mechanical brain injury. Stab injury to the neonatal 
      brain evoked neither MCP-1 expression nor astrogliosis. These results demonstrate 
      that chemokine gene expression comprises one component of the astrocyte 
      activation program. The data are consistent with a role for MCP-1 in the central 
      nervous system inflammatory response to trauma.
FAU - Glabinski, A R
AU  - Glabinski AR
AD  - Department of Neurosciences, Cleveland Clinic Foundation, OH 44195, USA.
FAU - Balasingam, V
AU  - Balasingam V
FAU - Tani, M
AU  - Tani M
FAU - Kunkel, S L
AU  - Kunkel SL
FAU - Strieter, R M
AU  - Strieter RM
FAU - Yong, V W
AU  - Yong VW
FAU - Ransohoff, R M
AU  - Ransohoff RM
LA  - eng
GR  - R01-32151/PHS 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  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Astrocytes/*immunology/metabolism
MH  - Brain/immunology/metabolism
MH  - Brain Injuries/genetics/*immunology/metabolism
MH  - Chemokine CCL2/*genetics
MH  - Female
MH  - Gene Expression
MH  - Male
MH  - Mice
MH  - RNA, Messenger/genetics/metabolism
MH  - Wounds, Penetrating/genetics/immunology/metabolism
EDAT- 1996/06/01 00:00
MHDA- 1996/06/01 00:01
CRDT- 1996/06/01 00:00
PHST- 1996/06/01 00:00 [pubmed]
PHST- 1996/06/01 00:01 [medline]
PHST- 1996/06/01 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1996 Jun 1;156(11):4363-8.