Calcineurin and glial signaling: Neuroinflammation and beyond

Jennifer L. Furman, Christopher M. Norris

Research output: Contribution to journalReview articlepeer-review

69 Scopus citations

Abstract

Similar to peripheral immune/inflammatory cells, neuroglial cells appear to rely on calcineurin (CN) signaling pathways to regulate cytokine production and cellular activation. Several studies suggest that harmful immune/inflammatory responses may be the most impactful consequence of aberrant CN activity in glial cells. However, newly identified roles for CN in glutamate uptake, gap junction regulation, Ca2+ dyshomeostasis, and amyloid production suggest that CN's influence in glia may extend well beyond neuroinflammation. The following review will discuss the various actions of CN in glial cells, with particular emphasis on astrocytes, and consider the implications for neurologic dysfunction arising with aging, injury, and/or neurodegenerative disease.

Original languageEnglish
Article number158
JournalJournal of Neuroinflammation
Volume11
Issue number1
DOIs
StatePublished - Sep 10 2014

Bibliographical note

Funding Information:
Work supported by awards from the NIH (AG027297), the Kentucky Spinal Cord and Head Injury Research Trust (12-10A), and The Hazel Embry Research Fund to CMN and an award from the PhRMA Foundation to JLF.

Publisher Copyright:
© 2014 Furman and Norris; licensee BioMed Central Ltd.

Keywords

  • Alzheimer's disease
  • Amyloid
  • Astrocytes
  • Ca2+ regulation
  • Calcineurin
  • Gap junction
  • Glutamate
  • Neurodegeneration
  • Neuroinflammation

ASJC Scopus subject areas

  • Neuroscience (all)
  • Immunology
  • Neurology
  • Cellular and Molecular Neuroscience

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