Linked Life Data

14766802

Source:http://linkedlifedata.com/resource/pubmed/id/14766802

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-3-31
pubmed:abstractText
Neuronal loss via apoptosis is a key element in numerous neurodegenerative diseases. To avoid accumulation of apoptotic material, the remains of apoptotic cells should be degraded. It was suggested that microglial cells are phagocytosing and degrading apoptotic material. There is only limited information available concerning the fate of the remains of apoptotic neurons. In this study, we investigated the ability of microglial cells to take up and degrade neuronal apoptotic material. We isolated primary microglial cells and used apoptotic bodies of apoptotic neuron-like PC12 cells as a substrate. The apoptotic material was taken up and degraded within the microglial cells. The uptake is clearly activation dependent. We were able to demonstrate that the CD36 scavenger receptor is involved in the uptake of the apoptotic material via competition studies, antibody blockage, and use of a CD36 mutant rat strain. Blockage of other uptake mechanisms was also able to inhibit the uptake to some extent. Furthermore, we were able to demonstrate the role of the microglial lysosomal and proteasomal pathways in the degradation of proteins originating from apoptotic bodies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
743-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Neuronal apoptotic bodies: phagocytosis and degradation by primary microglial cells.
pubmed:affiliation
Neuroscience Research Center, Medical Faculty (Charité), Humboldt University, Berlin, Germany.
pubmed:publicationType
Journal Article