Absence of clinical correlates of diabetic retinopathy in the Ins2Akita retina. (21st May 2013)

• Record Type: Journal Article
• Authors: McLenachan, Samuel; Chen, Xiangting; McMenamin, Paul G; Rakoczy, Elizabeth P
• Is Part Of: Clinical & experimental ophthalmology. Volume 41:Number 6(2013)
• Page Start: 582
• Page End: 592
• Publication Date: 2013-05-21
• Subjects: Ophthalmology -- Periodicals; 617.7
• DOI: 10.1111/ceo.12084
• Languages: English
• ISSNs: 1442-6404

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <sec id="ceo12084-sec-0001" sec-type="section"> <title>Background</title> <p>The <italic>Ins2<sup>Akita</sup></italic> mouse has been reported to display retinal pathology degeneration associated with advanced diabetic retinopathy. In the present study, we monitored retinal changes in these mice to establish if this model displays clinical features associated with advanced diabetic retinopathy in human patients.</p> </sec> <sec id="ceo12084-sec-0002" sec-type="section"> <title>Methods</title> <p> <italic>Ins2<sup>Akita</sup></italic> mice (<italic>n</italic> = 55) on a C57Bl/6J background were monitored clinically from 9 to 25 weeks of age using a combination of scanning laser ophthalmoscopy, fluorescein angiography and optical coherence tomography. After clinical imaging, eyes were processed for immunostaining to examine microglial, astroglial and Muller glial responses to hyperglycaemia. To complement our optical coherence tomography imaging, retinal morphology and thicknesses were examined in high‐quality semi‐thin sections.</p> </sec> <sec id="ceo12084-sec-0003" sec-type="section"> <title>Results</title> <p>No retinal thinning or disruption of retinal architecture was observed by optical coherence tomography or resin histology in <italic>Ins2<sup>Akita</sup></italic> mice up to 6 months of age. In addition, no vascular changes were detected by fluorescein angiography or by scanning laser ophthalmoscopy. With the exception of microglial activation, reduced glial fibrillary acid protein expression in astrocytes and an increase in glial fibrillary acid protein expression by Muller cells, no other changes were observed in the <italic>Ins2<sup>Akita</sup></italic> retina.</p> </sec> <sec id="ceo12084-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Our results indicate that the classical clinical correlates of human diabetic retinopathy are absent in <italic>Ins2<sup>Akita</sup></italic> mice up to 6 months of age suggesting that either the histopathological processes underlying the development of diabetic retinopathy in this model require longer than 5 months of hyperglycaemia to result in disruption of retinal architecture or that advanced diabetic retinopathy is not a feature of the <italic>Ins2<sup>Akita</sup></italic> diabetic mouse.</p> </sec> </abstract>