Hypoxia ischemia-mediated cell death in neonatal rat brain.
The examination of Bcl-2-associated X protein (Bax) protein's role in the activation of cognate nuclear, mitochondrial and ER cell death signaling cascades and the resulting effects on cell death phenotype in the brain after neonatal hypoxia-ischemia (HI) requires an understanding of neonatal HI insult and progression, as well as, its dysfunctional outcomes. In addition, knowledge of key concepts of oxidative stress, a major injurious component of HI, and the different cell death phenotypes (i.e. apoptosis and necrosis) will aid the design of appropriate useful experimental paradigms. Here we discuss organelle cell death signaling cascades in the context of the different cell death phenotypes associated with animal models of neonatal hypoxia ischemia and tissue culture models used in the study of hypoxia ischemia, focusing on the intracellular shifts of the Bcl-2 associated X protein (Bax) in the hypoxic brain.
Gill
Martin B
MB
Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch at Galveston, 301 University Blvd., Galveston, TX 77555-1072, USA.
Perez-Polo
J Regino
JR
D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000473:pathology*; D016923:Cell Death; D002534:Hypoxia, Brain / Q000473:pathology*; D018384:Oxidative Stress; D051381:Rats; D015398:Signal Transduction; D051028:bcl-2-Associated X Protein / Q000502:physiology
D051028:bcl-2-Associated X Protein