Linked Life Data

19931516

Source:http://linkedlifedata.com/resource/pubmed/id/19931516

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-1-27
pubmed:abstractText
We have previously demonstrated that mutant mice bearing astrocytes deficient in glial fibrillary acidic protein (GFAP) exhibited typical spongiform degeneration and prion plaque deposition. However, it remains to be determined whether there are astrocyte-specific alterations in the reactive response of astrocytes. Herein, we analyzed morphological features of Gfap(-)(/)(-) reactive astrocytes. Light microscopic morphometry of mutant reactive astrocytes revealed reduced outlined cell area and shorter distances among expanded cell space but with larger nuclei. Electron microscopy revealed mutant cells containing very few and sparse glial filaments as well as abnormal cytoarchitecture of reactive astrocytic processes. Furthermore, paired cell formation appeared frequently. The results suggest that GFAP is necessary for morphological retention and distribution of reactive astrocytes during prion disease, and that there is a GFAP-dependent function of glial filaments in reactive astrocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1872-6240
pubmed:author
pubmed:copyrightInfo
(c) 2009 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
1312
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
156-67
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Role of GFAP in morphological retention and distribution of reactive astrocytes induced by scrapie encephalopathy in mice.
pubmed:affiliation
Laboratory of Molecular Endocrinology and Metabolism, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi, Maebashi, Gunma 371-8512, Japan. hgomi@showa.gunma-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't