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T.J. McFarland, B. Appukuttan, Y. Zhang, J.T. Stout; Up–Regulation of RTEF–1 in a Primate Model of Central Retinal Artery Occlusion (CRAO) . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4894.
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The transcriptional enhancer factor 1–related (RTEF–1) gene is a member of the TEA DNA binding gene family and is associated with stimulating expression of an assortment of genes, including VEGF. RTEF–1 was originally identified as a cardiac and skeletal muscle specific factor. We recently identified novel alternatively spliced transcripts of RTEF–1 within human retinal blood vessels and within the mouse eye, although its exact role is undetermined. We aim to explore whether ischemia effects the RTEF–1 in experimentally induced CRAO within the eye of a nonhuman primate.
A central retinal artery occlusion was induced in the right eye of a cynomolgus primate via Rose bengal–assisted laser occlusion technique (532nm laser); the left eye served as a control. Color photographs and fluorescein angiography (FA) were taken immediately after the procedure to confirm occlusion. Twenty–four hours after the CRAO was induced, color and FA photos were taken and retina, choroid, and iris tissue and RNA was obtained. RNA was isolated from the three tissue groups, quantified and followed by semi–quantitative RT–PCR for the RTEF–1 transcript.
Immediately after laser treatment fundoscopy revealed hypoperfusion with a characteristic "cherry red spot" in the macula. Angiography revealed a complete central retinal artery occlusion of the lasered eye. Semi–quantitative RT–PCR from equally loaded retina and choroid samples showed remarkable up–regulation of the full length RTEF–1 transcript in the CRAO eye when compared to the control eye. There was little difference seen in the relative levels of RTEF–1 in the iris samples.
The ischemic response associated with a central retinal artery occlusion is correlated with a dramatic up–regulation of RTEF–1 mRNA in the retina and choroid. This response may be crucial to downstream transcriptional control of various angiogenic factors, such as VEGF. Questions concerning the relative level of RTEF–1 up–regulation and whether expression of VEGF and other factors are altered in this CRAO model are of interest and will be investigated by real–time quantitative RT–PCR. Whether alternatively spliced RETF products exist and questions about their cellular location is under investigation.
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