Linked Life Data

19210118

Source:http://linkedlifedata.com/resource/pubmed/id/19210118

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-4-13
pubmed:abstractText
The expression of the neutrophil chemokine macrophage inflammatory protein-2 (MIP-2/CXCL2) and the monocyte chemokine monocyte chemotactic protein-1 (MCP-1/CCL2) have been described in glial cells in vitro but their origin following TBI has not been established. Furthermore, little is known of the modulation of these chemokines. Chemokine expression was investigated in male Sprague-Dawley rats following moderate lateral fluid percussion injury (LFPI). At 0, 4, 8, 12, and 24 h after injury, brains were harvested and MIP-2/CXCL2 and MCP-1/CCL2 levels measured by ELISA. To investigate the inhibition of chemokine expression a second cohort of animals received dexamethasone (1-15mg/kg), FK506 (1mg/kg), or vehicle, systemically, immediately after injury. These animals were sacrificed at the time of peak chemokine expression. A third cohort of animals was also sacrificed at the time of peak chemokine expression and immunohistochemistry performed for MIP-2/CXCL2 and MCP-1/CCL2. Following LFPI, chemokines were increased in the ipsilateral hemisphere, MIP-2/CXCL2 peaking at 4 h and MCP-1/CCL2 peaking at 8-12 h post-injury. Dexamethasone significantly reduced cortical MCP-1/CCL2, but not MIP-2/CXCL2 concentrations. FK506 did not inhibit chemokine expression. In undamaged brain, chemokine expression was localized to cells with a neuronal morphology. For MIP-2/CXCL2 this was supported by double staining for the neuronal antigen NeuN. In contused tissue, increased MIP-2/CXCL2 and MCP-1/CCL2 staining was visible in cells with the morphology of degenerating neurons. MIP-2/CXCL2 and MCP-1/CCL2 are increased after injury, and neurons appear to be the source of this expression. Chemokine expression was selectively inhibited by dexamethasone. The implications of this are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1557-9042
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
507-25
pubmed:meshHeading
pubmed-meshheading:19210118-Animals, pubmed-meshheading:19210118-Anti-Inflammatory Agents, pubmed-meshheading:19210118-Brain, pubmed-meshheading:19210118-Brain Injuries, pubmed-meshheading:19210118-Chemokine CCL2, pubmed-meshheading:19210118-Chemokine CXCL2, pubmed-meshheading:19210118-Dexamethasone, pubmed-meshheading:19210118-Disease Models, Animal, pubmed-meshheading:19210118-Down-Regulation, pubmed-meshheading:19210118-Immunosuppressive Agents, pubmed-meshheading:19210118-Male, pubmed-meshheading:19210118-Nerve Degeneration, pubmed-meshheading:19210118-Nerve Tissue Proteins, pubmed-meshheading:19210118-Neurons, pubmed-meshheading:19210118-Nuclear Proteins, pubmed-meshheading:19210118-Rats, pubmed-meshheading:19210118-Rats, Sprague-Dawley, pubmed-meshheading:19210118-Tacrolimus, pubmed-meshheading:19210118-Time Factors, pubmed-meshheading:19210118-Up-Regulation
pubmed:year
2009
pubmed:articleTitle
The temporal expression, cellular localization, and inhibition of the chemokines MIP-2 and MCP-1 after traumatic brain injury in the rat.
pubmed:affiliation
University of Edinburgh, Department of Anaesthesia, Critical Care and Pain Medicine, Western General Hospital, Edinburgh, Scotland. J.K.J.Rhodes@sms.ed.ac.uk
pubmed:publicationType
Journal Article