Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2379-2389 |
| Number of pages | 11 |
| Journal | Neurochemical Research |
| Volume | 33 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 2008 |
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Keywords
- Apoptosis
- Bax
- Cell death
- Hypoxia
- Ischemia
- Low birth weight babies
- Necrosis
- Neonatal
- Organelles
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Biochemistry
Cite this
Hypoxia ischemia-mediated cell death in neonatal rat brain. / Gill, Martin B.; Perez-Polo, J. Regino.
In: Neurochemical Research, Vol. 33, No. 12, 12.2008, p. 2379-2389.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hypoxia ischemia-mediated cell death in neonatal rat brain
AU - Gill, Martin B.
AU - Perez-Polo, J. Regino
PY - 2008/12
Y1 - 2008/12
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Bax
KW - Cell death
KW - Hypoxia
KW - Ischemia
KW - Low birth weight babies
KW - Necrosis
KW - Neonatal
KW - Organelles
UR - http://www.scopus.com/inward/record.url?scp=56349117483&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=56349117483&partnerID=8YFLogxK
U2 - 10.1007/s11064-008-9649-1
DO - 10.1007/s11064-008-9649-1
M3 - Article
VL - 33
SP - 2379
EP - 2389
JO - Neurochemical Research
JF - Neurochemical Research
SN - 0364-3190
IS - 12
ER -