These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Proteomic identification of carbonylated proteins in the monkey hippocampus after ischemia-reperfusion.
    Author: Oikawa S, Yamada T, Minohata T, Kobayashi H, Furukawa A, Tada-Oikawa S, Hiraku Y, Murata M, Kikuchi M, Yamashima T.
    Journal: Free Radic Biol Med; 2009 Jun 01; 46(11):1472-7. PubMed ID: 19272443.
    Abstract:
    Reactive oxygen species (ROS) are known to participate in neurodegeneration after ischemia-reperfusion. With the aid of ROS, the calpain-induced lysosomal rupture provokes ischemic neuronal death in the cornu Ammonis (CA) 1 of the hippocampus; however, the target proteins of ROS still remain unknown. Here a proteomic analysis was done to identify and characterize ROS-induced carbonyl modification of proteins in the CA1 of the macaque monkey after transient whole-brain ischemia followed by reperfusion. We found that carbonyl modification of heat shock 70-kDa protein 1 (Hsp70-1), a major stress-inducible member of the Hsp70 family, was extensively increased before the neuronal death in the CA1 sector, and the carbonylation site was identified to be Arg469 of Hsp70-1. The CA1 neuronal death conceivably occurs by calpain-mediated cleavage of carbonylated Hsp70 that becomes prone to proteolysis with the resultant lysosomal rupture. In addition, the carbonyl levels of dihydropyrimidinase-like 2 isoform 2, glial fibrillary acidic protein, and beta-actin were remarkably increased in the postischemic CA1. Therefore, ischemia-reperfusion-induced oxidative damage to these proteins in the CA1 may lead to loss of the neuroprotective function, which contributes to neuronal death.
    [Abstract] [Full Text] [Related] [New Search]