| Literature DB >> 19103253 |
Hee-Kwon Park1, Kon Chu, Keun-Hwa Jung, Soon-Tae Lee, Jae-Joon Bahn, Manho Kim, Sang Kun Lee, Jae-Kyu Roh.
Abstract
Autophagy is a key pathway for the clearance of damaged organelles. Ischemic preconditioning (IPC) and autophagy are enhanced by mild hypoxic insults, but the association between autophagy and IPC remains unclear. We investigated the existence and role of autophagy in IPC. In an in vitro PC12 cell model, IPC increased generation and degradation of autophagosomes, as revealed by increased LC3-II bands, cathepsin D positive cells, lysosomal activity and autophagic vacuoles on electron microscopy. Autophagic activity was blocked using 3-methyladenine during IPC, and cell viabilities were measured using FASC and WST-1 assays. Inhibition of autophagy, especially during reperfusion or lethal oxygen-glucose deprivation periods ameliorated the neuroprotective effects of IPC. Moreover, inhibiting autophagy also attenuated Hsp70 upregulation induced by IPC. These findings imply that autophagy participates in IPC-induced neuroprotection, and that autophagy might provide a means of neuroprotection against cerebral ischemia.Entities:
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Year: 2008 PMID: 19103253 DOI: 10.1016/j.neulet.2008.12.019
Source DB: PubMed Journal: Neurosci Lett ISSN: 0304-3940 Impact factor: 3.046