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TAT‐BH4 counteracts Aβ toxicity on capillary endothelium
Author(s) -
Cantara S.,
Thorpe P.E.,
Ziche M.,
Donnini S.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.01.037
Subject(s) - oxidative stress , apoptosis , programmed cell death , caspase , endothelium , amyloid beta , nitric oxide , microbiology and biotechnology , endothelial stem cell , chemistry , peptide , senile plaques , biology , pathology , medicine , biochemistry , alzheimer's disease , endocrinology , disease , in vitro
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.