Document Detail


Transient acidification and subsequent proinflammatory cytokine stimulation of astrocytes induce distinct activation phenotypes.
MedLine Citation:
PMID:  23154943     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The foot processes of astrocytes cover over 60% of the surface of brain microvascular endothelial cells, regulating tight junction integrity. Retraction of astrocyte foot processes has been postulated to be a key mechanism in pathology. Therefore, movement of an astrocyte in response to a proinflammatory cytokine or even limited retraction of processes would result in leaky junctions between endothelial cells. Astrocytes lie at the gateway to the CNS and are instrumental in controlling leukocyte entry. Cultured astrocytes typically have a polygonal morphology until stimulated. We hypothesized that cultured astrocytes which were induced to stellate would have an activated phenotype compared with polygonal cells. We investigated the activation of astrocytes derived from adult macaques to the cytokine TNF-α under resting and stellated conditions by four parameters: morphology, intermediate filament expression, adhesion, and cytokine secretion. Astrocytes were stellated following transient acidification; resulting in increased expression of GFAP and vimentin. Stellation was accompanied by decreased adhesion that could be recovered with proinflammatory cytokine treatment. Surprisingly, there was decreased secretion of proinflammatory cytokines by stellated astrocytes compared with polygonal cells. These results suggest that astrocytes are capable of multiple phenotypes depending on the stimulus and the order stimuli are applied.
Authors:
Nicole A Renner; Hope A Sansing; Fiona M Inglis; Smriti Mehra; Deepak Kaushal; Andrew A Lackner; Andrew G Maclean
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  228     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2013 Jun 
Date Detail:
Created Date:  2013-02-26     Completed Date:  2013-04-18     Revised Date:  2014-06-03    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1284-94     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
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MeSH Terms
Descriptor/Qualifier:
Animals
Astrocytes / drug effects,  immunology,  metabolism*
Biological Markers / metabolism
Buffers
Cell Adhesion
Cell Shape
Cells, Cultured
Cytokines / genetics,  metabolism*
Female
Gene Expression Regulation
Glial Fibrillary Acidic Protein / metabolism
HEPES / pharmacology
Hydrogen-Ion Concentration
Inflammation Mediators / metabolism*
Intermediate Filaments / metabolism
Macaca mulatta
Male
Neural Cell Adhesion Molecules / metabolism
Phenotype
Time Factors
Vimentin / metabolism
Grant Support
ID/Acronym/Agency:
MH077544/MH/NIMH NIH HHS; OD11104/OD/NIH HHS; P20RR16816/RR/NCRR NIH HHS; P51 OD011104/OD/NIH HHS; P51 RR000164/RR/NCRR NIH HHS; R01 MH077544/MH/NIMH NIH HHS; RR00164/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Buffers; 0/Cytokines; 0/Glial Fibrillary Acidic Protein; 0/Inflammation Mediators; 0/Neural Cell Adhesion Molecules; 0/Vimentin; RWW266YE9I/HEPES
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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