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A. Muniz, H. D. Yarbrough, P. R. Edsall, B. E. Stuck, H.-C. H. Wang; A Mouse Model of Retinal Laser Injury With Apoptotic Photoreceptor Cell Death. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4467.
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© ARVO (1962-2015); The Authors (2016-present)
Laser use in medical, industrial and military settings results in accidental laser retinal injury. No treatment for laser eye injury exists and little is known concerning the biology of laser induced photoreceptor cell death. This study is to establish a model for the mechanistic study of cellular damage by investigating three parameters: laser intensity, time-dependent peak of apoptosis, and morphologic development of lesion characteristics within retinal tissue and thereby characterize a mouse laser retinal injury model.
Anesthetized C57BL/C mice received retinal lesions by 0.1s exposure to a multi-line Argon laser dose of 60, 120 and 150mW; 100µm spot size. Eyes harvested at 3, 8, 24, 48 and 72 hours were prepared by frozen section and examined morphologically by light microscopy. In situ labeling of apoptotic cells by terminal dUTP nick end labeling (TUNEL) was performed to detect apoptosis-specific internucleosomal DNA fragmentation.
Apoptosis peaks at 24 hours in retinas exposed to 120 and 150mW doses. No apoptotic photoreceptors were seen at 3 hours for all three doses. At 8 hours, apoptotic photoreceptors were noticeable in 120 and 150mW lesions. At 24 hours the number of apoptosis positive photoreceptors peaked and then decreased by 48 hours and were lightly visible by 72 hours in the 120mW and 150mW lesions. No reproducible photoreceptor apoptosis was detected in the 60mW lesions. Lesions produced by 150mW caused severe morphologic disruption. There was a dose-dependent relative increase in the number of apoptotic cells within lesions, as well as severity of morphologic lesion characteristics within the tissues.
This study showed that laser exposure directly induced apoptotic photoreceptor cell death. Apoptosis can be observed within 8 hours. Lesions presented in the 120mW exposure are optimal, providing both characteristic lesion morphology and photoreceptor cell death. The reproducible characteristics of this model will make it a useful tool to evaluate neuroprotective pharmaceuticals and neuroregenerative therapies.
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