Expression profiling of neuroinflammatory genes in LPS and LPS/IFNγ-stimulated BV-2 microglia cells

In Su Kim, Ji Hwan Park, Jin Hwan Do, Hyun Myung Ko, Eun Jung Park, Kyoungho Suk, Dong Kug Choi

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

A large body of evidence indicates that microglia, resident innate immune cells in the brain, play a role in host defense and function as active contributors to neuron damage in neurodegenerative disease. Microglia are crucial in the immune response within the central nervous system(CNS), and function in protecting the brain against injury. In contrast, activated microglia can secrete numerous reactants that damage neurons. The pathogenesis of various neurodegenerative diseases has been associated with microglia activation. Elucidation of molecular mechanisms underlying microglia activation could aid in controlling neuroinflammation and subsequent neurodegeneration. To increase the understanding of microglia activation, a cDNA microarray was presently used to profile genome-wide expression in activated BV-2 microglia cells. The analysis revealed that genome expression was differentially modulated for 1.2% of the total cellular transcripts in lipopolysaccharide/interferon-γ (LPS/IFNγ)-activated BV-2 microglia cells. Comparison of array data between LPS- and LPS/IFNγ-activated cells showed that the transcriptional signature was similarly regulated. This common expression pattern of stimulation was statistically significant, with > 2-fold change evident for 38 genes. To evaluate the functional significance of the altered gene expression in microglia cells, PBEF1, an induced gene both LPS and LPS/IFNγ-activated BV-2 microglia, was further analyzed in a 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine-intoxicated animal model.

Original languageEnglish
Pages (from-to)299-305
Number of pages7
JournalBiochip Journal
Volume3
Issue number4
StatePublished - 2009

Keywords

  • Interferon gamma
  • Lipopolysaccharide
  • Microarray analysis
  • Microglia
  • Neuroinflammation

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