Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-4-19
pubmed:abstractText
In this study we evaluated the activation of the cytokine and growth factor responsive transcription factors signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NFkappaB) after different grades of neural damage in the immature rat brain using double immunocytochemical techniques and electron microscopy. Following neocortical N-methyl-D-aspartate induced excitotoxic cell death, both these transcription factors are mainly activated in astrocytes, although microglia, endothelial cells, and neurons show transient activation at specific times and locations. Interestingly, activation of both transcription factors is only observed in cortical areas affected by severe tissue damage, neuronal degeneration, and blood-brain barrier (BBB) disruption. In contrast, the milder glial response occurring in the distal thalamus is not preceded by immunocytochemically detectable STAT3 and NFkappaB activation, although microglial response, astroglial hypertrophy, and glial fibrillary acidic protein (GFAP) overexpression do occur. In the cortex, astrocytes show STAT3 and NFkappaB activation already at 2 to 4 hours post-lesion, preceding cell hypertrophy and GFAP upregulation, and being maintained in the long-term formed glial scar. STAT3 and NFkappaB activation in microglial cells is protracted and observed at 10 to 24 hours post-lesion. The early activation of both transcription factors in astroglial cells could contribute to the changes in gene expression leading to astrogliosis and the release of signalling molecules which may contribute to the subsequent activation of these transcription factors in microglial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
151-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
STAT3 and NFkappaB activation precedes glial reactivity in the excitotoxically injured young cortex but not in the corresponding distal thalamic nuclei.
pubmed:affiliation
School of Medicine, Department of Cell Biology, Physiology and Immunology, Autonomous University of Barcelona, Bellaterra, Spain.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't