Transplantation of human neural stem cells protect against ischemia in a preventive mode via hypoxia-inducible factor-1alpha stabilization in the host brain

Brain Res. 2008 May 1:1207:182-92. doi: 10.1016/j.brainres.2008.02.043. Epub 2008 Mar 4.

Abstract

Hypoxia-inducible factor-1 (HIF-1) plays important roles in the prevention of cerebral ischemia. Deferoxamine (DFX), an iron chelator stabilizes the HIF-1alpha and activates target genes involved in compensation for ischemia. In this study, we are to investigate whether HIF-1alpha can be stabilized in human neural stem cells (NSCs) by DFX, and pre-transplantation of NSCs with HIF-1alpha stabilization can induce prolonged ischemic tolerance. In the DFX-treated NSCs, the HIF-1alpha protein expression was increased about 100-fold time-dependently, and subsequent transcriptional activation (VEGF, BDNF and CXCR4) was also observed. To test an ability to induce ischemic prevention in vivo, DFX-treated NSCs or naïve NSCs were transplanted in the striatum of adult rats. Seven days following the transplantation, focal cerebral ischemia was done. Infarct volumes were reduced in both NSCs-transplanted groups, compared with ischemia-only, but more reduced in DFX-treated NSCs group. The protective effects of NSCs were ablated when HIF-1alpha was silenced. HIF-1alpha protein levels were increased in both NSCs-transplanted groups, but more increased in DFX-treated NSCs group. RT-PCR analysis manifested a downregulation of mRNA expression of TNF-alpha, IL-6 and MMP-9 in both NSCs groups, but further decrease in DFX-treated NSCs group. These findings provide evidence that HIF-1alpha stabilization in human NSCs can be achieved effectively by DFX, and HIF-1alpha-stabilized NSCs protect against ischemia in a preventive mode.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / metabolism
  • Brain / surgery
  • Brain Infarction / prevention & control
  • Brain Ischemia / pathology
  • Brain Ischemia / prevention & control
  • Brain Ischemia / surgery*
  • Chemokine CXCL12 / pharmacology
  • Cyclooxygenase 2 / metabolism
  • Deferoxamine / pharmacology
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Flow Cytometry / methods
  • Gene Expression Regulation / drug effects
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / drug effects
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
  • Neurons / drug effects
  • Neurons / physiology*
  • Rats
  • Receptors, CXCR4 / metabolism
  • Siderophores / pharmacology
  • Stem Cell Transplantation / methods*
  • Stem Cells / drug effects
  • Stem Cells / physiology*
  • Time Factors
  • Up-Regulation / physiology
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • CXCR4 protein, human
  • Chemokine CXCL12
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Receptors, CXCR4
  • Siderophores
  • Vascular Endothelial Growth Factor A
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Deferoxamine