Linked Life Data

12797382

Source:http://linkedlifedata.com/resource/pubmed/id/12797382

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-6-11
pubmed:abstractText
Eph receptors and ligands represent two families of proteins that control axonal guidance during development. Recent work has shown that several Eph receptors are expressed postnatally. Because the Eph molecules represent a class of axon guidance molecules that are mainly inhibitory to axonal growth, we investigated whether EphB3 expression was upregulated in both spinal cord and four supraspinal nuclei (locus coeruleus, vestibular, raphe pallidus, and red) 1 week after a complete spinal cord thoracic transection. Injured rats had a significant increase in EphB3 mRNA and protein expression in the spinal cord. The increased EphB3 expression was colocalized with GFAP staining and indicated that astrocytes play a role in EphB3 expression after spinal cord injury. No change in EphB3 expression was seen in supraspinal brain nuclei, which further demonstrated that changes in expression were due to changes in the local microenvironment at the injury site. The expression of EphB3 was colocalized to regions of the CNS that had a high level of EphB3 binding ligands. These data indicate upregulation of EphB3 expression after injury may also contribute to an environment in the spinal cord that is inhibitory to axonal regeneration.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0963-6897
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
279-90
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Transection of the adult rat spinal cord upregulates EphB3 receptor and ligand expression.
pubmed:affiliation
Kentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't