Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C0022116 (
ischemia
)
91,303
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Brain ischemic injury is associated with clinical emergencies such as acute ischemic and hemorrhagic stroke, head trauma, prolonged severe hypotension and cardiac arrest. Ischemic preconditioning (IPC) is the most powerful endogenous mechanism against ischemic injury. However, the majority of IPC treatments are invasive and thus impractical in the clinical setting. Identifying the endogenous neuroprotective mechanism induced by IPC is important for developing new strategies to reduce stroke severity.
Zinc finger protein 667
(
ZNF667
) is a novel zinc finger protein that is upregulated by myocardial IPC. However, its functional role in neuronal
ischemia
has not been elucidated. In this study, the changes of
ZNF667
expression on cerebral IPC and its potential neuroprotective function were investigated. The cerebral ischemia model was established by ameliorated four-vessel occlusion in rats. The northern blot results demonstrated that
ZNF667
expression was increased in the hippocampus and cortex at 12 and 24 h after cerebral ischemic pretreatment. To investigate the neuroprotective function of
ZNF667
, enhanced green fluorescent protein (EGFP)-
ZNF667
fusion protein was expressed in C2C12 and brain astrocytoma cells and its subcellular localization was detected by confocal microscopy. EGFP-
ZNF667
fusion proteins were localized in the nucleus of C2C12 and brain astrocytoma cells, indicating that
ZNF667
may act as a transcription factor in neural cells. To mimic oxidative stress associated with
ischemia
/reperfusion injury, hydrogen peroxide (H
2
O
2
) was used to treat cells. Cell viability was measured by the lactate dehydrogenase (LDH) and WST-1 assays. A decrease in viability was detected in C2C12 and astrocytoma cells following H
2
O
2
treatment, whereas
ZNF667
gene overexpression significantly improved cell viability following H
2
O
2
treatment. These results suggested that
ZNF667
plays a neuroprotective role by acting as a transcription factor in cerebral IPC.
...
PMID:Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress. 2464 81
