TAT-BH4 counteracts Aβ toxicity on capillary endothelium
- 24 January 2007
- journal article
- Published by Wiley in FEBS Letters
- Vol. 581 (4) , 702-706
- https://doi.org/10.1016/j.febslet.2007.01.037
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 Abeta-induced apoptotic cell death by activating a survival programme which is Akt/endothelial nitric oxide synthase dependent.Keywords
This publication has 16 references indexed in Scilit:
- Critical role of actin in modulating BBB permeabilityBrain Research Reviews, 2005
- Amyloid β induces neuronal cell death through ROS-mediated ASK1 activationCell Death & Differentiation, 2004
- Mechanisms of Soluble β-Amyloid Impairment of Endothelial FunctionJournal of Biological Chemistry, 2004
- Exogenous BH4/Bcl-2 Peptide Reverts Coronary Endothelial Cell Apoptosis Induced by Oxidative StressJournal of Vascular Research, 2004
- BH4-domain peptide from Bcl-xL exerts anti-apoptotic activity in vivoOncogene, 2003
- Cerebral Microvessel Responses to Focal IschemiaJournal of Cerebral Blood Flow & Metabolism, 2003
- β‐Amyloid inhibits NOS activity by subtracting NADPH availabilityThe FASEB Journal, 2002
- Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosomeNature, 2002
- Amyloid β Peptide–Induced Cerebral Endothelial Cell Death Involves Mitochondrial Dysfunction and Caspase ActivationJournal of Cerebral Blood Flow & Metabolism, 2001
- Nitric Oxide Is an Upstream Signal of Vascular Endothelial Growth Factor-induced Extracellular Signal-regulated Kinase½ Activation in Postcapillary EndotheliumJournal of Biological Chemistry, 1998