Abstract
Purpose: :
Flicker at ~20 HZ has been reported to decrease or delay the development of experiment myopia. In this experiment, we undertook a genome-wide analysis of the early transcriptional response of C57/6J mouse retinas to flicker as well as form-deprivation.
Methods: :
fifty-four C57/6J mice were randomly divided into three groups: form-deprivation-only (FD+/FL-), form-deprivation & flickering illumination (FD+/FL+), and control (FD-/FL-). The right eyes of mice in the first two groups were covered with diffusers to impose form-deprivation, while the contralateral eyes were left open for clear vision as self control. Both eyes of mice in the control group were left uncovered. The mice in the FD+/FL- group and the control group were raised in normal light, whereas the mice in the FD+/FL+ group were exposed to 25HZ flicker. At the end of the treatment (t=1 hour), mice were sacrificed and retinas were prepared to Affymetrix GeneChip Mouse Genome 430 2.0 arrays, data were analyzed by Genespring 10.0 (Unpaired T-Test,P<0.05).
Results: :
(1) The response to form-deprivation alone: 1147 genes were found to change their expression. Possible significant pathways involved included JNK cascade, TGF-signaling pathway (through TAK1), and lipid and lipoprotein metabolism. (2) The influence of flicker on response to form-deprivation: 749 genes were found to change their expression. Possible significant pathways involved included JNK cascade and activated Rap 1 signaling et al; (3) The response may involve in myopia: Assuming that flicker suppresses myopia in mice, it could do so by inhibiting the expression of genes related to myopia, holding them near normal control levels. 84 genes of this kind were detected; their functions are mainly involved with the iron ion.
Conclusions: :
Gene Microarray analysis could provide many new candidate genes related to myopia. This study also helps to elucidate the mechanism by which flicker inhibits myopia development.
Keywords: myopia • gene microarray • retina