IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

(Investigative Ophthalmology and Visual Science. 2007;48:405-411.)
© 2007 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.06-0854
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Appendices
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smit-McBride, Z.
Right arrow Articles by Hjelmeland, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smit-McBride, Z.
Right arrow Articles by Hjelmeland, L. M.

A Strong Genetic Determinant of Hyperoxia-Related Retinal Degeneration on Mouse Chromosome 6

Zeljka Smit-McBride,1 Sharon L. Oltjen,1 Matthew M. LaVail,2 and Leonard M. Hjelmeland1

1From the Department of Ophthalmology, Vitreoretinal Research Lab, University of California at Davis, School of Medicine, Davis, California; and the 2Beckman Vision Center, University of California, San Francisco School of Medicine, San Francisco, California.

PURPOSE. Hyperoxia-related retinal degeneration (HRRD) is a model system in the mouse in which elevated oxygen levels are used to induce retinal degeneration. The hypothesis for the present study was that strain differences in HRRD susceptibility are due to allelic variants of one or more genes in the mouse genome whose human orthologues should be important targets for research and drug development.

METHODS. C57BL/6J, A/J, or B.A-Chr6 mice were exposed to 75% oxygen (hyperoxia) or room air for 14 days. After death, one eye was fixed and processed for outer nuclear layer (ONL) thickness measurements. The retina and RPE/choroid were separately dissected from the fellow eye and processed for microarray analysis. Single nucleotide polymorphism (SNP) analysis for transcribed sequences from the C57BL/6J and A/J genomes was conducted using the NIH genome site.

RESULTS. C57BL/6J mice developed a significant retinal degeneration in the inferior hemisphere after 14 days of hyperoxia. Under identical conditions, A/J mice exhibited only minor changes. A significant genetic effect was located on chromosome 6. SNP analysis of known transcribed sequences on chromosome 6 combined with microarray expression analysis yielded 33 candidate genes.

CONCLUSIONS. A significant genetic effect of susceptibility to HRRD is located on chromosome 6. In silico analysis of transcribed sequences results in a fairly small number of candidate genes.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the Association for Research in Vision and Ophthalmology