Linked Life Data

15051517

Source:http://linkedlifedata.com/resource/pubmed/id/15051517

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-3-30
pubmed:abstractText
The hypothesis that devascularization of somatosensory and motor cortex causes apoptosis in infarcted regions and in the linked thalamic nuclei was evaluated. To unravel whether Bcl-related proteins, known to regulate apoptosis, participate in neuronal and glial responses to devascularization, we analyzed immunohistochemically the distribution and intensity of staining of Bcl-2 and Bax proteins at different time points after lesion. Both early (up to 6 h) and late (1-7 days) responses were studied. Devascularization led to rapid (within hours) apoptosis in the cortex and to a delayed (within 3-7 days) apoptosis in thalamic nuclei. In control groups, Bcl-2 and Bax immunoreactivity (IR) was detected in neurons and oligodendrocytes but not in astrocytes or microglia. Following devascularization, Bcl-2 IR and Bax IR increased in neurons before the onset of the apoptosis. In the ischemic focus, the increase reached maximal values 3 h after the lesion. The increase was of slower onset in the penumbra zone (24 h and after), a region in which both proteins were induced in astrocytes also. The change of Bax IR intensity exceeded four times that of Bcl-2 at all time points investigated, indicating a diminution of Bcl-2/Bax ratio that may direct neurons to apoptotic pathway. In numerous neurons, an increase of IR in the cytoplasm was accompanied by induction of nuclear staining. No changes of Bcl-2 and Bax IR were found in thalamic nuclei. Our results point to different mechanisms underlying apoptosis of cortical and thalamic neurons. Nuclear appearance of Bcl-2 and Bax suggests they possess regulatory role of gene expression changes triggered by cortical infarct.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
1006
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-49
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15051517-Animals, pubmed-meshheading:15051517-Apoptosis, pubmed-meshheading:15051517-Cell Count, pubmed-meshheading:15051517-Cerebral Cortex, pubmed-meshheading:15051517-Glial Fibrillary Acidic Protein, pubmed-meshheading:15051517-Immunohistochemistry, pubmed-meshheading:15051517-In Situ Nick-End Labeling, pubmed-meshheading:15051517-Ischemic Attack, Transient, pubmed-meshheading:15051517-Male, pubmed-meshheading:15051517-Neocortex, pubmed-meshheading:15051517-Neurons, pubmed-meshheading:15051517-Oligodendroglia, pubmed-meshheading:15051517-Phosphopyruvate Hydratase, pubmed-meshheading:15051517-Proteins, pubmed-meshheading:15051517-Proto-Oncogene Proteins, pubmed-meshheading:15051517-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:15051517-Rats, pubmed-meshheading:15051517-Rats, Wistar, pubmed-meshheading:15051517-Staining and Labeling, pubmed-meshheading:15051517-Thalamus, pubmed-meshheading:15051517-Time Factors, pubmed-meshheading:15051517-bcl-2-Associated X Protein
pubmed:year
2004
pubmed:articleTitle
Bcl-2 and Bax proteins are increased in neocortical but not in thalamic apoptosis following devascularizing lesion of the cerebral cortex in the rat: an immunohistochemical study.
pubmed:affiliation
Laboratory for Reinnervation Processes, Department of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur St., 02-093 Warsaw, Poland.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't