Acute isolation and transcriptome characterization of cortical astrocytes and microglia from young and aged mice

Marie Orre, Willem Kamphuis, Lana M. Osborn, Jeroen Melief, Lieneke Kooijman, Inge Huitinga, Jan Klooster, Koen Bossers, Elly M. Hol*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

15 Citations (Scopus)

Abstract

Astrocytes and microglia become reactive in many neurological disorders resulting in phenotypic and functional alterations. Both cell types might also display functional changes during normal aging. To identify gene signatures and changes in basal cellular functions of astrocytes and microglia in relation to aging, we isolated viable astrocytes and microglia from young adult and aged mouse cortices and determined their gene expression profile. Aged astrocytes, compared with young astrocytes, showed an increased inflammatory phenotype and increased `zinc ion binding.' Young astrocytes showed higher expression of genes involved in `neuronal differentiation' and hemoglobin synthesis. Astrocyte expression of genes involved in neuronal signaling remains high throughout age. Aged microglia had higher expression of genes involved in `vesicle release,' `zinc ion binding,' and genes within the tumor necrosis factor-ligand family and young microglia had increased transcript levels of C-C motif chemokines. These data provide a transcriptome database of cell-type enriched genes of astrocytes and microglia from adult mice and give insight into the differential gene signature of astrocytes and microglia in relation to normal aging. (c) 2014 Elsevier Inc. All rights reserved.

Original languageEnglish
Pages (from-to)1-14
Number of pages14
JournalNeurobiology of Aging
Volume35
Issue number1
DOIs
Publication statusPublished - Jan 2014
Externally publishedYes

Keywords

  • Cell isolation
  • Astrocytes
  • Microglia
  • Aging
  • Transcriptome
  • Tripartite synapse
  • Immune signaling
  • CENTRAL-NERVOUS-SYSTEM
  • IN-VIVO
  • DOPAMINERGIC-NEURONS
  • ALZHEIMERS-DISEASE
  • REACTIVE GLIOSIS
  • SELF-RENEWAL
  • AGING BRAIN
  • G-PROTEIN
  • CELLS
  • ACTIVATION

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