Linked Life Data

12605885

Source:http://linkedlifedata.com/resource/pubmed/id/12605885

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-2-27
pubmed:abstractText
Reports on non-neural cells have shown that enhanced activity of the Ca(2+)-dependent/ATP-independent phospholipid scramblase (PLSCR1) is, at least in part, responsible for surface exposure of phosphatidylserine and the collapse of plasma membrane asymmetry in injured or apoptotic cells. To shed some light on mechanisms with a potential to lead to apoptotic death of human neurones following ischemic/hypoxic injury, we examined the immunoreactivity of hippocampal neurones for PLSCR1, caspase-3, cytochrome c and DNA-fragmentation in 22 individuals with clinically symptomatic cerebral ischemia after cardiac arrest or severe hypotension. WE FOUND: (1) significant differences in the percentage of PLSCR1-immunoreactive neurones between controls and short survivors; statistically strong differences between the frequency of immunoreactive neurones among the subfields studied with lowest levels in the CA3; preferential distribution of immunoreactive neurones in controls within the regio entorhinalis, subfield CA1, and hilum. Additionally, these areas exhibited staining of fibre bundles which probably correspond to perforant path, alvear path and collateral's of Schaffer, (2) caspase-3 was upregulated in a region-specific manner with marked activation in the selectively vulnerable hippocampal areas, (3) cytochrome c was redistributed, (4) DNA-fragmentation represented by scattered TUNEL-positive cells increased predominantly during the first 3 days after ischemia, and particularly in the regions of greatest susceptibility to hypoxic injury. This study presents the first evidence that PLSCR1, and probably remodelling of plasma membrane phospholipids (PL), plays a role in ischemic injury in the human hippocampus.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0197-0186
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
79-87
pubmed:dateRevised
2009-11-3
pubmed:meshHeading
pubmed-meshheading:12605885-Adult, pubmed-meshheading:12605885-Aged, pubmed-meshheading:12605885-Apoptosis, pubmed-meshheading:12605885-Autopsy, pubmed-meshheading:12605885-Brain Ischemia, pubmed-meshheading:12605885-Carrier Proteins, pubmed-meshheading:12605885-Caspase 3, pubmed-meshheading:12605885-Caspases, pubmed-meshheading:12605885-Cell Count, pubmed-meshheading:12605885-Cell Death, pubmed-meshheading:12605885-Cytochrome c Group, pubmed-meshheading:12605885-DNA Fragmentation, pubmed-meshheading:12605885-Enzyme Activation, pubmed-meshheading:12605885-Female, pubmed-meshheading:12605885-Hippocampus, pubmed-meshheading:12605885-Humans, pubmed-meshheading:12605885-Immunohistochemistry, pubmed-meshheading:12605885-In Situ Nick-End Labeling, pubmed-meshheading:12605885-Male, pubmed-meshheading:12605885-Membrane Proteins, pubmed-meshheading:12605885-Middle Aged, pubmed-meshheading:12605885-Phospholipid Transfer Proteins
pubmed:year
2003
pubmed:articleTitle
Spatial resolution of phospholipid scramblase 1 (PLSCR1), caspase-3 activation and DNA-fragmentation in the human hippocampus after cerebral ischemia.
pubmed:affiliation
Anatomisches Institut III, Universitätsklinikum, Theodor-Stern-Kai 7, 60590, Frankfurt/Main, Germany. rami@em.uni-frankfurt.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't