Sandra Zinkel
Assistant Professor of Medicine
Last active: 3/26/2019

Function of BID -- a molecule of the bcl-2 family -- in ischemic cell death in the brain.

Plesnila N, Zinkel S, Amin-Hanjani S, Qiu J, Korsmeyer SJ, Moskowitz MA
Eur Surg Res. 2002 34 (1-2): 37-41

PMID: 11867899 · DOI:10.1159/000048885

Mitochondrial mechanisms, particularly the release of cytochrome c, play a role in the death of nerve and glial cells in cerebral ischemia. We have currently investigated whether BID, a proapoptotic molecule of the bcl-2 family and promoter of the release of cytochrome c is expressed in the brain, activated by cerebral ischemia in vivo, and contributes to ischemic cell death. We found BID in the cytosol of mouse brain and of primary cultured mouse neurons and showed that neuronal BID is a substrate for caspase 8. BID was cleaved in vivo 4 h after transitory occlusion of the middle cerebral artery. Further, BID(-/-) mice had a significant attenuation of infarction (-67%) and significantly lower release of cytochrome c (-41%). The findings indicate that the proapoptotic molecule BID may contribute to the demise of nerve cells from cerebral ischemia by release of cytochrome c and activation of caspase.

Copyright 2002 S. Karger AG, Basel

MeSH Terms (13)

Animals Apoptosis BH3 Interacting Domain Death Agonist Protein Brain Ischemia Carrier Proteins Cytochrome c Group Gene Expression Mice Mice, Inbred C57BL Mice, Knockout Phenotype Proto-Oncogene Proteins c-bcl-2 Rats

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