Source:http://linkedlifedata.com/resource/pubmed/id/18723055
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0001613,
umls-concept:C0007776,
umls-concept:C0022116,
umls-concept:C0022655,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0035124,
umls-concept:C0376515,
umls-concept:C0521390,
umls-concept:C0552510,
umls-concept:C1314792,
umls-concept:C1514559,
umls-concept:C1533691,
umls-concept:C1545588
|
pubmed:issue |
2
|
pubmed:dateCreated |
2008-9-8
|
pubmed:abstractText |
Recent studies have suggested that neuronal apoptosis in cerebral ischemia could arise from dysfunction of endoplasmic reticulum (ER) and mitochondria. B-cell lymphoma/leukemia-2 gene (Bcl-2) has been described as an inhibitor both in programmed cell death (PCD) and ER dysfunction during apoptosis, and the Bcl-2 family play a key role in regulating the PCD, both locally at the ER and from a distance at the mitochondrial membrane. However, its signal pathways and concrete mechanisms in endoplasmic reticulum-initiated apoptosis remain incompletely understood. We therefore investigate whether ischemia/reperfusion (I/R) causes neuronal apoptosis in part via cross-talk between ER and mitochondria or not, and how the overexpression of Bcl-2 prevents this form of cell death. Here we show that analogous I/R-induced cell death occurs consequent to interactions of ER stress and mitochondrial death pathways. The participation of the mitochondrial pathway was demonstrated by the release of cytochrome C (cyt C) from mitochondrial into cytoplasmic fractions and caspase-9 cleavage. The involvement of ER stress was further supported by the observable increase of glucose-regulated protein 78(GRP78)/BiP expression and caspase-12 activity. Furthermore, prior to these changes, swelling of the ER lumen and dissociation of ribosomes from rough ER were detected by electron microscopy. Bcl-2 overexpression inhibits the release of cyt C and the activation of caspase-9/-8/-3 but not caspase-12 based on the results of Western blot. These suggest that cross-talk between ER and mitochondria participate in neuronal damage after ischemia/reperfusion. Bcl-2 overexpression could suppress I/R-induced neuronal apoptosis via influencing mitochondrial integrity.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0168-0102
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
62
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
140-6
|
pubmed:meshHeading |
pubmed-meshheading:18723055-Animals,
pubmed-meshheading:18723055-Apoptosis,
pubmed-meshheading:18723055-Blotting, Western,
pubmed-meshheading:18723055-Caspases,
pubmed-meshheading:18723055-Cells, Cultured,
pubmed-meshheading:18723055-Cerebral Cortex,
pubmed-meshheading:18723055-Cytochromes c,
pubmed-meshheading:18723055-Endoplasmic Reticulum,
pubmed-meshheading:18723055-Microscopy, Electron, Transmission,
pubmed-meshheading:18723055-Mitochondria,
pubmed-meshheading:18723055-Neurons,
pubmed-meshheading:18723055-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:18723055-Rats,
pubmed-meshheading:18723055-Rats, Sprague-Dawley,
pubmed-meshheading:18723055-Reperfusion Injury,
pubmed-meshheading:18723055-Signal Transduction,
pubmed-meshheading:18723055-Up-Regulation
|
pubmed:year |
2008
|
pubmed:articleTitle |
The protection of Bcl-2 overexpression on rat cortical neuronal injury caused by analogous ischemia/reperfusion in vitro.
|
pubmed:affiliation |
Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, China.
|
pubmed:publicationType |
Journal Article
|