Journal
BRAIN BEHAVIOR AND IMMUNITY
Volume 24, Issue 5, Pages 822-830Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2009.09.013
Keywords
Apoptosis; Bax; Neuronal death; Immuno-electron microscopy; Perinatal
Categories
Funding
- Swedish Research Council
- Swedish Childhood Cancer Foundation
- Sweden-Japan Foundation
- Frimurare Barnhus Foundation
- Gothenburg Medical Society
- Ahlen Foundation
- Swedish Society of Medicine
- Wilhelm and Martina Lundgren Foundation
- Sven Jerring Foundation
- Magnus Bergvall Foundation
- Action Medical Research [1764] Funding Source: researchfish
- Medical Research Council [G0802853] Funding Source: researchfish
- MRC [G0802853] Funding Source: UKRI
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Apoptosis-related mechanisms are important in the pathophysiology of hypoxic-ischemic injury in the neonatal brain. Caspases are the major executioners of apoptosis, but there are a number of upstream players that influence the cell death pathways. The Bcl-2 family proteins are important modulators of mitochondrial permeability, working either to promote or prevent apoptosis. In this study we focused on the anti-apoptotic Bcl-2 protein after neonatal cerebral hypoxia-ischemia (HI) in 8-day-old rats. Bcl-2 translocated to nuclei and accumulated there over the first 24 h of reperfusion after HI, as judged by immunohistochemistry and immuno-electron microscopy. We also found that the total level of Bcl-2 decreased after HI in vivo and after ionophore challenge in cultured human neuroblastoma (IMR-32) cells in vitro. Furthermore, the Bcl-2 reduction was calpain-dependent, because it could be prevented by the calpain inhibitor CX295 both in vivo and in vitro, suggesting cross-talk between excitotoxic and apoptotic mechanisms. (C) 2009 Elsevier Inc. All rights reserved.
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