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

Producción científica: Review article › revisión exhaustiva

99 Citas (Scopus)

Resumen

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.

Idioma original	English
Número de artículo	158
Publicación	Journal of Neuroinflammation
Volumen	11
N.º	1
DOI	https://doi.org/10.1186/s12974-014-0158-7
Estado	Published - sept 10 2014

Nota bibliográfica

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

Financiación

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.

Financiadores	Número del financiador
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

ASJC Scopus subject areas

General Neuroscience
Immunology
Neurology
Cellular and Molecular Neuroscience

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title = "Calcineurin and glial signaling: Neuroinflammation and beyond",

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.

KW - Alzheimer's disease

KW - Amyloid

KW - Astrocytes

KW - Ca2+ regulation

KW - Calcineurin

KW - Gap junction

KW - Glutamate

KW - Neurodegeneration

KW - Neuroinflammation

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DO - 10.1186/s12974-014-0158-7

M3 - Review article

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Calcineurin and glial signaling: Neuroinflammation and beyond

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

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