期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 24, 期 11, 页码 1219-1225出版社
SAGE PUBLICATIONS INC
DOI: 10.1097/01.WCB.0000136706.77918.21
关键词
ubiquitin; brain ischemia; postsynaptic density; electron microscopy
资金
- NINDS NIH HHS [R29 NS036810, R56 NS036810, R01 NS040407, P50 NS030291, R01 NS036810] Funding Source: Medline
- PHS HHS [MS36810] Funding Source: Medline
The mechanisms underlying neurologic deficits and delayed neuronal death after ischemia are not fully understood. In the present study, we report that transient cerebral ischemia induces accumulation of ubiquitinated proteins (ubi-proteins) in postsynaptic densities (PSDs). By immuno-electron microscopy, we demonstrated that ubi-proteins were highly accumulated in PSD structures after ischemia. On Western blots, ubi-proteins were markedly increased in purified PSDs at 30 minutes of reperfusion, and the increase persisted until cell death in the CA1 region after ischemia. In the resistant DG area, however, the changes were transient and significantly less pronounced. Deposition of ubi-proteins in PSDs after ischemia correlates well with PSD structural damage in the CA1 region as viewed by electron microscopy. These results suggest that the ubiquitin-proteasome system fails to repair and remove damaged proteins in PSDs. The changes may demolish synaptic neurotransmission, contribute to neurologic deficits, and eventually lead to delayed neuronal death after transient cerebral ischemia.
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