Location of Repository

Neuroprotection by hypoxic preconditioning requires sequential activation of vascular endothelial growth factor receptor and Akt

By Antje Wick, Wolfgang Wick, Johannes Waltenberger, Michael Weller, Johannes Dichgans and Jörg B. Schulz

Abstract

Hypoxic preconditioning provides protection against ischemic brain lesions in animal models of cerebral ischemia–hypoxia. To analyze the underlying molecular mechanisms, we developed an in vitro model of hypoxic neuroprotection in cerebellar granule neurons (CGN) by reducing the oxygen tension to 1–5 % for 1–24 hr. Exposure to 5 % O 2 for 9 hr resulted in reduction of cell death after potassium deprivation, treatment with 100 �M glutamate, or 500 �M 3-nitroproprioninc acid (3-NP) by 46, 22, and 55%, respectively. Shorter (1 or 3 hr) or longer (�12 hr) intervals or pretreatment with lower oxygen tension failed to rescue CGN from death. In contrast, toxicity of four different chemotherapeutic drugs [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea, cisplatine, topotecane, and vincristine] was unaffected by hypoxic preconditioning. The induction of protective effects was dependent on new protein synthesis. Protein levels of B-cell lymphom

Year: 2013
OAI identifier: oai:CiteSeerX.psu:10.1.1.320.5525
Provided by: CiteSeerX
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://citeseerx.ist.psu.edu/v... (external link)
  • http://www.jneurosci.org/conte... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.