Linked Life Data

13680276

Source:http://linkedlifedata.com/resource/pubmed/id/13680276

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-11-7
pubmed:abstractText
Cerebrovascular white matter lesions represent an age-related neurodegenerative condition that appears as a hyperintense signal on magnetic resonance images. These lesions are frequently observed in aging, hypertension and cerebrovascular disease, and are responsible for cognitive decline and gait disorders in the elderly population. In humans, cerebrovascular white matter lesions are accompanied by apoptosis of oligodendroglia, and have been thought to be caused by chronic cerebral ischemia. In the present study, we tested whether chronic cerebral hypoperfusion induces white matter lesions and apoptosis of oligodendroglia in the rat. Doppler flow meter analysis revealed an immediate reduction of cerebral blood flow ranging from 30% to 40% of that before operation; this remained at 52-64% between 7 and 30 days after operation. Transferrin-immunoreactive oligodendroglia decreased in number and the myelin became degenerated in the medial corpus callosum at 7 days and thereafter. Using the TUNEL method, the number of cells showing DNA fragmentation increased three- to eightfold between 3 and 30 days post-surgery compared to sham-operated animals. Double labeling with TUNEL and immunohistochemistry for markers of either astroglia or oligodendroglia showed that DNA fragmentation occurred in both of these glia. Messenger RNA for caspase-3 increased approximately twofold versus the sham-operated rats between 1 and 30 days post-surgery. Immunohistochemistry revealed up-regulation of caspase-3 in the oligodendroglia of the white matter, and also in the astroglia and neurons of the gray matter. Molecules involved in apoptotic signaling such as TNF-alpha and Bax were also up-regulated in glial cells. These results indicate that chronic cerebral hypoperfusion induces white matter degeneration in association with DNA fragmentation in oligodendroglia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0001-6322
pubmed:author
pubmed:issnType
Print
pubmed:volume
106
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
527-34
pubmed:dateRevised
2007-11-9
pubmed:meshHeading
pubmed-meshheading:13680276-Animals, pubmed-meshheading:13680276-Blotting, Northern, pubmed-meshheading:13680276-Brain Ischemia, pubmed-meshheading:13680276-Caspase 3, pubmed-meshheading:13680276-Caspases, pubmed-meshheading:13680276-Cerebral Cortex, pubmed-meshheading:13680276-DNA Fragmentation, pubmed-meshheading:13680276-Immunohistochemistry, pubmed-meshheading:13680276-In Situ Nick-End Labeling, pubmed-meshheading:13680276-Laser-Doppler Flowmetry, pubmed-meshheading:13680276-Male, pubmed-meshheading:13680276-Oligodendroglia, pubmed-meshheading:13680276-Proto-Oncogene Proteins, pubmed-meshheading:13680276-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:13680276-RNA, Messenger, pubmed-meshheading:13680276-Rats, pubmed-meshheading:13680276-Rats, Wistar, pubmed-meshheading:13680276-Time Factors, pubmed-meshheading:13680276-Tumor Necrosis Factor-alpha, pubmed-meshheading:13680276-Up-Regulation, pubmed-meshheading:13680276-bcl-2-Associated X Protein
pubmed:year
2003
pubmed:articleTitle
Chronic cerebral hypoperfusion induces white matter lesions and loss of oligodendroglia with DNA fragmentation in the rat.
pubmed:affiliation
Department of Neurology, Faculty of Medicine, Kyoto University, Sakyo-ku, 606-8507, Kyoto. tomimoto@kuhp.kyoto-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't