Abstract
Oxidative stress is one of the factor contributing to blood brain barrier degeneration. This phenomenon is observed during pathological conditions such as Alzheimer's disease or cerebral amyloid angiopathy in which brain haemorrhages are very frequent. Both diseases are characterized by beta amyloid peptide deposition either in neurons or in vessels. Oxidative stress leads to impairment of mitochondrial functions and apoptotic cell death subsequent to caspases activation. In this paper we demonstrate that BH4 domain of Bcl-xl administrated to endothelial cells as the conjugated form with TAT peptide, reverts Aβ-induced apoptotic cell death by activating a survival programme which is Akt/endothelial nitric oxide synthase dependent.
Original language | English (US) |
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Pages (from-to) | 702-706 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 581 |
Issue number | 4 |
DOIs | |
State | Published - Feb 20 2007 |
Keywords
- Apoptosis
- Beta amyloid
- Cerebral amyloid angiopathy
- Endothelium
- TAT-BH4
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology