Document Detail


MCP-1 involvement in glial differentiation of neuroprogenitor cells through APP signaling.
MedLine Citation:
PMID:  19185603     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previously it has been reported that neural stem cells undergoing apoptotic stress have increased levels of amyloid precursor protein (APP) and increased APP expression results in glial differentiation. APP activity was also shown to be required for staurosporine-induced glial differentiation of neuroprogenitor cells. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that is expressed early during inflammation. The binding of MCP-1 to its chemokine receptor induces expression of novel transcription factor MCP-1-induced protein (MCPIP). MCPIP expression subsequently leads to cell death. Previous studies have shown that pro-apoptotic factors have the ability to induce neural differentiation. Therefore, we investigated if MCPIP expression leads to differentiation of NT2 neuroprogenitor cells. Results showed that MCPIP expression increased glial fibrillary acid protein (GFAP) expression and also caused distinct morphological changes, both indicative of glial differentiation. Similar results were observed with MCP-1 treatment. Interestingly, APP expression decreased in response to MCPIP. Instead, we found APP activity regulates expression of both MCP-1 and MCPIP. Furthermore, inhibition of either p38 MAPK or JAK signaling pathways significantly reduced APP's effect on MCP-1 and MCPIP. These data demonstrates the role APP has in glial differentiation of NT2 cells through MCP-1/MCPIP signaling. It is possible that increased APP expression after CNS injury could play a role in MCP-1 production, possibly promoting astrocyte activation at injured site.
Authors:
Emmanuel George Vrotsos; Pappachan E Kolattukudy; Kiminobu Sugaya
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-01-29
Journal Detail:
Title:  Brain research bulletin     Volume:  79     ISSN:  1873-2747     ISO Abbreviation:  Brain Res. Bull.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-23     Completed Date:  2009-04-28     Revised Date:  2012-09-27    
Medline Journal Info:
Nlm Unique ID:  7605818     Medline TA:  Brain Res Bull     Country:  United States    
Other Details:
Languages:  eng     Pagination:  97-103     Citation Subset:  IM    
Affiliation:
Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816-2364, USA.
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MeSH Terms
Descriptor/Qualifier:
Amyloid beta-Protein Precursor / metabolism*
Cell Death / physiology
Cell Differentiation* / physiology
Cell Line
Chemokine CCL2 / metabolism*
Glial Fibrillary Acidic Protein / metabolism
Humans
Janus Kinases / metabolism
MAP Kinase Signaling System
Neuroglia / cytology,  physiology*
Phosphorylation
Protease Nexins
RNA, Messenger / metabolism
Receptors, Cell Surface / metabolism*
STAT3 Transcription Factor / metabolism
Signal Transduction
Stem Cells / physiology*
Transcription Factors / metabolism*
p38 Mitogen-Activated Protein Kinases / metabolism
Grant Support
ID/Acronym/Agency:
AG 23472/AG/NIA NIH HHS; R01 AG023472-01/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/APP protein, human; 0/Amyloid beta-Protein Precursor; 0/CCL2 protein, human; 0/Chemokine CCL2; 0/Glial Fibrillary Acidic Protein; 0/Protease Nexins; 0/RNA, Messenger; 0/Receptors, Cell Surface; 0/STAT3 Transcription Factor; 0/STAT3 protein, human; 0/Transcription Factors; 0/ZC3H12A protein, human; EC 2.7.10.2/Janus Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases
Comments/Corrections

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