Systems Biology Profiling of AMD on the Basis of Gene Expression
Genetic pathways underlying the initiation and progression of age-related macular degeneration (AMD) have not been yet sufficiently revealed, and the correlations of AMD’s genotypes, phenotypes, and disease spectrum are still awaiting resolution. We are tackling both problems with systems biology ph...
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Language: | English |
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Wiley
2013-01-01
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Series: | Journal of Ophthalmology |
Online Access: | http://dx.doi.org/10.1155/2013/453934 |
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author | Mones S. Abu-Asab Jose Salazar Jingsheng Tuo Chi-Chao Chan |
author_facet | Mones S. Abu-Asab Jose Salazar Jingsheng Tuo Chi-Chao Chan |
author_sort | Mones S. Abu-Asab |
collection | DOAJ |
description | Genetic pathways underlying the initiation and progression of age-related macular degeneration (AMD) have not been yet sufficiently revealed, and the correlations of AMD’s genotypes, phenotypes, and disease spectrum are still awaiting resolution. We are tackling both problems with systems biology phylogenetic parsimony analysis. Gene expression data (GSE29801: NCBI, Geo) of macular and extramacular specimens of the retinas and retinal pigment epithelium (RPE) choroid complexes representing dry AMD without geographic atrophy (GA), choroidal neovascularization (CNV), GA, as well as pre-AMD and subclinical pre-AMD were polarized against their respective normal specimens and then processed through the parsimony program MIX to produce phylogenetic cladograms. Gene lists from cladograms’ nodes were processed in Genomatix GePS to reveal the affected signaling pathway networks. Cladograms exposed a highly heterogeneous transcriptomic profiles within all the conventional phenotypes. Moreover, clades and nodal synapomorphies did not support the classical AMD phenotypes as valid transcriptomal genotypes. Gene lists defined by cladogram nodes showed that the AMD-related deregulations occurring in the neural retina were different from those in RPE-choroidal tissue. Our analysis suggests a more complex transcriptional profile of the phenotypes than expected. Evaluation of the disease in much earlier stages is needed to elucidate the initial events of AMD. |
format | Article |
id | doaj-art-dbeba200d8e942dfadd17a46f90c6399 |
institution | Kabale University |
issn | 2090-004X 2090-0058 |
language | English |
publishDate | 2013-01-01 |
publisher | Wiley |
record_format | Article |
series | Journal of Ophthalmology |
spelling | doaj-art-dbeba200d8e942dfadd17a46f90c63992025-02-03T01:31:28ZengWileyJournal of Ophthalmology2090-004X2090-00582013-01-01201310.1155/2013/453934453934Systems Biology Profiling of AMD on the Basis of Gene ExpressionMones S. Abu-Asab0Jose Salazar1Jingsheng Tuo2Chi-Chao Chan3Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USALaboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USALaboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USALaboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USAGenetic pathways underlying the initiation and progression of age-related macular degeneration (AMD) have not been yet sufficiently revealed, and the correlations of AMD’s genotypes, phenotypes, and disease spectrum are still awaiting resolution. We are tackling both problems with systems biology phylogenetic parsimony analysis. Gene expression data (GSE29801: NCBI, Geo) of macular and extramacular specimens of the retinas and retinal pigment epithelium (RPE) choroid complexes representing dry AMD without geographic atrophy (GA), choroidal neovascularization (CNV), GA, as well as pre-AMD and subclinical pre-AMD were polarized against their respective normal specimens and then processed through the parsimony program MIX to produce phylogenetic cladograms. Gene lists from cladograms’ nodes were processed in Genomatix GePS to reveal the affected signaling pathway networks. Cladograms exposed a highly heterogeneous transcriptomic profiles within all the conventional phenotypes. Moreover, clades and nodal synapomorphies did not support the classical AMD phenotypes as valid transcriptomal genotypes. Gene lists defined by cladogram nodes showed that the AMD-related deregulations occurring in the neural retina were different from those in RPE-choroidal tissue. Our analysis suggests a more complex transcriptional profile of the phenotypes than expected. Evaluation of the disease in much earlier stages is needed to elucidate the initial events of AMD.http://dx.doi.org/10.1155/2013/453934 |
spellingShingle | Mones S. Abu-Asab Jose Salazar Jingsheng Tuo Chi-Chao Chan Systems Biology Profiling of AMD on the Basis of Gene Expression Journal of Ophthalmology |
title | Systems Biology Profiling of AMD on the Basis of Gene Expression |
title_full | Systems Biology Profiling of AMD on the Basis of Gene Expression |
title_fullStr | Systems Biology Profiling of AMD on the Basis of Gene Expression |
title_full_unstemmed | Systems Biology Profiling of AMD on the Basis of Gene Expression |
title_short | Systems Biology Profiling of AMD on the Basis of Gene Expression |
title_sort | systems biology profiling of amd on the basis of gene expression |
url | http://dx.doi.org/10.1155/2013/453934 |
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