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.
Document Type
Article
Publication Date
9-10-2014
Digital Object Identifier (DOI)
http://dx.doi.org/10.1186/s12974-014-0158-7
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.
Repository Citation
Furman, Jennifer L. and Norris, Christopher M., "Calcineurin and Glial Signaling: Neuroinflammation and Beyond" (2014). Sanders-Brown Center on Aging Faculty Publications. 51.
https://uknowledge.uky.edu/sbcoa_facpub/51
Notes/Citation Information
Published in Journal of Neuroinflammation, v. 11, article 158, p. 1-12.
© 2014 Furman and Norris; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.