TAT-BH4 counteracts Aβ toxicity on capillary endothelium

S. Cantara, P. E. Thorpe, M. Ziche, S. Donnini

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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 languageEnglish (US)
Pages (from-to)702-706
Number of pages5
JournalFEBS Letters
Issue number4
StatePublished - Feb 20 2007


  • Apoptosis
  • Beta amyloid
  • Cerebral amyloid angiopathy
  • Endothelium
  • TAT-BH4

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


Dive into the research topics of 'TAT-BH4 counteracts Aβ toxicity on capillary endothelium'. Together they form a unique fingerprint.

Cite this