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Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1
BACKGROUND: The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure (IOP) and glaucoma. We have shown previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iri...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1937007/ https://www.ncbi.nlm.nih.gov/pubmed/17608931 http://dx.doi.org/10.1186/1471-2156-8-45 |
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author | Howell, Gareth R Libby, Richard T Marchant, Jeffrey K Wilson, Lawriston A Cosma, Ioan M Smith, Richard S Anderson, Michael G John, Simon WM |
author_facet | Howell, Gareth R Libby, Richard T Marchant, Jeffrey K Wilson, Lawriston A Cosma, Ioan M Smith, Richard S Anderson, Michael G John, Simon WM |
author_sort | Howell, Gareth R |
collection | PubMed |
description | BACKGROUND: The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure (IOP) and glaucoma. We have shown previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iris disease. However, mechanisms involved in the subsequent IOP elevation and optic nerve degeneration remain unclear. RESULTS: Here we present new mouse strains with Gpnmb and/or Tyrp1 genes of normal function and with a DBA/2J genetic background. These strains do not develop elevated IOP or glaucoma with age. CONCLUSION: These strains provide much needed controls for studying pathogenic mechanisms of glaucoma using DBA/2J mice. Given the involvement of Gpnmb and/or Tyrp1 in areas such as immunology and tumor development and progression, these strains are also important in other research fields. |
format | Text |
id | pubmed-1937007 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-19370072007-08-02 Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 Howell, Gareth R Libby, Richard T Marchant, Jeffrey K Wilson, Lawriston A Cosma, Ioan M Smith, Richard S Anderson, Michael G John, Simon WM BMC Genet Research Article BACKGROUND: The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure (IOP) and glaucoma. We have shown previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iris disease. However, mechanisms involved in the subsequent IOP elevation and optic nerve degeneration remain unclear. RESULTS: Here we present new mouse strains with Gpnmb and/or Tyrp1 genes of normal function and with a DBA/2J genetic background. These strains do not develop elevated IOP or glaucoma with age. CONCLUSION: These strains provide much needed controls for studying pathogenic mechanisms of glaucoma using DBA/2J mice. Given the involvement of Gpnmb and/or Tyrp1 in areas such as immunology and tumor development and progression, these strains are also important in other research fields. BioMed Central 2007-07-03 /pmc/articles/PMC1937007/ /pubmed/17608931 http://dx.doi.org/10.1186/1471-2156-8-45 Text en Copyright © 2007 Howell et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Howell, Gareth R Libby, Richard T Marchant, Jeffrey K Wilson, Lawriston A Cosma, Ioan M Smith, Richard S Anderson, Michael G John, Simon WM Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 |
title | Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 |
title_full | Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 |
title_fullStr | Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 |
title_full_unstemmed | Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 |
title_short | Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1 |
title_sort | absence of glaucoma in dba/2j mice homozygous for wild-type versions of gpnmb and tyrp1 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1937007/ https://www.ncbi.nlm.nih.gov/pubmed/17608931 http://dx.doi.org/10.1186/1471-2156-8-45 |
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