Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
BMC Genomics. 2008 Feb 8;9:73. doi: 10.1186/1471-2164-9-73.

Analysis of the retinal gene expression profile after hypoxic preconditioning identifies candidate genes for neuroprotection.

Author information

  • 1Lab of Retinal Cell Biology, Dept Ophthalmology, University of Zurich, Switzerland. markus.thiersch@usz.ch

Abstract

BACKGROUND:

Retinal degeneration is a main cause of blindness in humans. Neuroprotective therapies may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1alpha in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration. To address the molecular mechanisms of the protection, we analyzed the transcriptome of the hypoxic retina using microarrays and real-time PCR.

RESULTS:

Hypoxic exposure induced a marked alteration in the retinal transcriptome with significantly different expression levels of 431 genes immediately after hypoxic exposure. The normal expression profile was restored within 16 hours of reoxygenation. Among the differentially regulated genes, several candidates for neuroprotection were identified like metallothionein-1 and -2, the HIF-1 target gene adrenomedullin and the gene encoding the antioxidative and cytoprotective enzyme paraoxonase 1 which was previously not known to be a hypoxia responsive gene in the retina. The strongly upregulated cyclin dependent kinase inhibitor p21 was excluded from being essential for neuroprotection.

CONCLUSION:

Our data suggest that neuroprotection after hypoxic preconditioning is the result of the differential expression of a multitude of genes which may act in concert to protect visual cells against a toxic insult.

PMID:
18261226
[PubMed - indexed for MEDLINE]
PMCID:
PMC2270833
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for BioMed Central Icon for PubMed Central
    Loading ...
    Write to the Help Desk