GFAP-independent inflammatory competence and trophic functions of astrocytes generated from murine embryonic stem cells

Glia. 2012 Feb;60(2):218-28. doi: 10.1002/glia.21257. Epub 2011 Nov 9.

Abstract

The directed generation of pure astrocyte cultures from pluripotent stem cells has proven difficult. Generation of defined pluripotent-stem-cell derived astrocytes would allow new approaches to the investigation of plasticity and heterogeneity of astrocytes. We here describe a two-step differentiation scheme resulting in the generation of murine embryonic stem cell (mESC) derived astrocytes (MEDA), as characterized by the upregulation of 19 astrocyte-associated mRNAs, and positive staining of most cells for GFAP (glial fibrillary acidic protein), aquaporin-4 or glutamine synthetase. The MEDA cultures could be cryopreserved, and they neither contained neuronal, nor microglial cells. They also did not react to the microglial stimulus lipopolysaccharide, while inflammatory activation by a complete cytokine mix (CCM) or its individual components (TNF-α, IL1-β, IFN-γ) was readily observed. MEDA, stimulated by CCM, became susceptible to CD95 ligand-induced apoptosis and produced NO and IL-6. This was preceded by NF-kB activation, and up-regulation of relevant mRNAs. Also GFAP-negative astrocytes were fully inflammation-competent. Neurotrophic support by MEDA was found to be independent of GFAP expression. In summary, we described here the generation and functional characterization of microglia-free murine astrocytes, displaying phenotypic heterogeneity as is commonly observed in brain astrocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects
  • Astrocytes / metabolism
  • Astrocytes / pathology*
  • Cell Culture Techniques / methods*
  • Cell Differentiation / genetics*
  • Cell Line
  • Cell Lineage / genetics
  • Embryonic Stem Cells / cytology
  • Embryonic Stem Cells / metabolism
  • Embryonic Stem Cells / pathology*
  • Glial Fibrillary Acidic Protein / deficiency
  • Glial Fibrillary Acidic Protein / physiology*
  • Inflammation / metabolism
  • Inflammation / pathology*
  • Mice
  • Mice, Inbred BALB C
  • Nerve Growth Factors / metabolism*
  • Phenotype
  • Primary Cell Culture

Substances

  • Glial Fibrillary Acidic Protein
  • Nerve Growth Factors