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Experimental & Molecular Medicine ; : 495-504, 2008.
Article in English | WPRIM | ID: wpr-84653

ABSTRACT

Exposure to light can induce photoreceptor cell death and exacerbate retinal degeneration. In this study, mice with genetic knockout of several genes, including rhodopsin kinase (Rhok-/-), arrestin (Sag-/-), transducin (Gnat1-/-), c-Fos (c-Fos-/-) and arrestin/transducin (Sag-/-/Gnat1-/-), were examined. We measured the expression levels of thousands of genes in order to investigate their roles in phototransduction signaling in light-induced retinal degeneration using DNA microarray technology and then further explored the gene network using pathway analysis tools. Several cascades of gene components were induced or inhibited as a result of corresponding gene knockout under specific light conditions. Transducin deletion blocked the apoptotic signaling induced by exposure to low light conditions, and it did not require c-Fos/AP-1. Deletion of c-Fos blocked the apoptotic signaling induced by exposure to high intensity light. In the present study, we identified many gene transcripts that are essential for the initiation of light-induced rod degeneration and proposed several important networks that are involved in pro- and anti-apoptotic signaling. We also demonstrated the different cascades of gene components that participate in apoptotic signaling under specific light conditions.


Subject(s)
Animals , Mice , Apoptosis/radiation effects , G-Protein-Coupled Receptor Kinase 1/genetics , GTP-Binding Protein alpha Subunits/genetics , Gene Expression Profiling , Genes, fos/genetics , Light/adverse effects , Light Signal Transduction/genetics , Mice, Knockout , Oligonucleotide Array Sequence Analysis , Retina/metabolism , Retinal Degeneration/etiology , Transducin/genetics
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