Calcineurin and glial signaling: Neuroinflammation and beyond

Jennifer L. Furman; Christopher M. Norris

doi:10.1186/s12974-014-0158-7

Calcineurin and glial signaling: Neuroinflammation and beyond

Jennifer L. Furman, Christopher M. Norris

Research output: Contribution to journal › Review article › peer-review

86 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 language	English
Article number	158
Journal	Journal of Neuroinflammation
Volume	11
Issue number	1
DOIs	https://doi.org/10.1186/s12974-014-0158-7
State	Published - Sep 10 2014

Bibliographical note

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

Funding

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.

Funders	Funder number
Hazel Embry Research Fund
National Institutes of Health (NIH)
National Institutes of Health (NIH)
National Institute on Aging	R01AG027297
Pharmaceutical Research and Manufacturers of America Foundation
Kentucky Spinal Cord and Head Injury Research Trust	12-10A

Keywords

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

ASJC Scopus subject areas

General Neuroscience
Immunology
Neurology
Cellular and Molecular Neuroscience

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10.1186/s12974-014-0158-7

Cite this

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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.",

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AB - 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.

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Calcineurin and glial signaling: Neuroinflammation and beyond

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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