Document Detail


Egr1 expression is induced following glatiramer acetate immunotherapy in rodent models of glaucoma and Alzheimer's disease.
MedLine Citation:
PMID:  21969301     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: Immunization with glatiramer acetate (GA) alleviates the neuropathology associated with glaucoma and Alzheimer's disease (AD) in rodent models. This research was undertaken to screen for molecular factors underlying GA-induced neuroprotective mechanisms in these models of chronic neurodegeneration.
METHODS: Gene expression profiles were analyzed in GA-immunized versus nonimmunized elevated-intraocular pressure (IOP) rat models of glaucoma by using whole genome cDNA microarrays and were further validated by quantitative real-time PCR analysis. A gene, prominently upregulated by GA in elevated IOP retina, was further studied in APP(SWE)/PS1(ΔE9)-transgenic (AD-Tg) mice after GA immunization.
RESULTS: Seven days after treatment with GA, numerous genes were regulated in the retinas of rats with elevated IOP. Comprehensive functional classification and DAVID/KEGG enrichment analysis of GA-induced differentially expressed genes revealed annotation terms and pathways involved in neuroprotection, immune responses, cell communication, and regeneration. Specifically, increased mRNA levels of an early growth response (Egr) 1 gene were evident in GA-immunized retinas with elevated IOP. In AD-Tg mice, a significant increase in hippocampal EGR1 protein levels was also found in response to GA immunization. Nuclear EGR1 in the dentate gyrus colocalized more frequently with doublecortin-positive and Ki67 proliferating neural progenitors in GA-immunized as compared to nonimmunized AD-Tg mice. Further, EGR1 levels were negatively correlated with hippocampal amyloid-β plaque burden.
CONCLUSIONS: This study presents global gene expression profiles associated with GA immunization in a glaucoma rat model. Moreover, it identifies EGR1 transcription factor as a potential mediator for GA-induced neuroprotection in both glaucoma and AD.
Authors:
Sharon Bakalash; Michael Pham; Yosef Koronyo; Brenda C Salumbides; Andrei Kramerov; Hillary Seidenberg; Dror Berel; Keith L Black; Maya Koronyo-Hamaoui
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-11-21
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  52     ISSN:  1552-5783     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-22     Completed Date:  2012-01-16     Revised Date:  2013-01-09    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  9033-46     Citation Subset:  IM    
Affiliation:
Department of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts, USA.
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MeSH Terms
Descriptor/Qualifier:
Alzheimer Disease / drug therapy*,  genetics,  immunology
Animals
Chronic Disease
Disease Models, Animal
Early Growth Response Protein 1 / genetics*
Female
Gene Expression / drug effects,  immunology
Glaucoma / drug therapy*,  genetics,  immunology
Hippocampus / physiology
Immunosuppressive Agents / pharmacology*
Male
Mice
Mice, Transgenic
Nerve Degeneration / drug therapy,  genetics,  immunology
Neuroprotective Agents / pharmacology
Oligonucleotide Array Sequence Analysis
Peptides / pharmacology*
Rats
Rats, Inbred Lew
Real-Time Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Early Growth Response Protein 1; 0/Egr1 protein, mouse; 0/Egr1 protein, rat; 0/Immunosuppressive Agents; 0/Neuroprotective Agents; 0/Peptides; 0/copolymer 1

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


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