Abstract
Retinal degeneration is a progressive retinal damage in ocular vascular diseases. There are several reasons for this, such as occlusion of arteries or veins, diabetic retinopathy, or hereditary retinal diseases. To study pathological mechanisms of retinal degeneration, it is required to develop experimentally reproducible and clinically relevant models. In our previous studies, we developed a murine model of retinal hypoperfusion by unilateral common carotid artery occlusion (UCCAO) which mimics the pathophysiology of ocular ischemic syndrome (OIS) in humans, and described broad pathological mechanisms in the retina after UCCAO. However, there still remain missing pieces of the ocular pathologic process by UCCAO. In this study, we examined those unfound mechanisms. UCCAO was performed on adult mice. Ocular dysfunctions, histological deficits, and inflammation were examined after UCCAO, compared with sham-operated mice. Evaluation values were analyzed by electrophysiological, histological, and molecular biological methods. Eyelid drooping was permanently seen after UCCAO. Induction time point of acute reversible cataract under anesthesia was shortened. Retinal/visual dysfunctions were detected 2-4 weeks after UCCAO. Specifically, scotopic b-wave was more affected than a-wave, with the dysfunction of photopic b-wave. Impaired oscillatory potentials and visual evoked potential were constantly observed. Pathological Müller gliosis/inflammation was featured with NeuN-positive cell loss in the ganglion cell layer. Axial length, intraocular pressure, pupillary light reflex, and retinal pigment epithelium/choroidal thickness were not changed by UCCAO. A murine model of retinal ischemia by UCCAO can be useful for studying a series of degenerative process in the ischemic retina.
Highlights
Retinal degeneration is a leading cause of incurable vision loss
There still remain missing pieces of the pathologic process in the unilateral common carotid artery occlusion (UCCAO)-operated eye, such as axial length, intraocular pressure (IOP), pupillary light reflex (PLR), acute reversible cataract under anesthesia, ocular function, the retinal pigment epithelium (RPE)/choroidal condition, pathological Müller gliosis, and inflammation. We examined those unfound mechanisms of retinal degenerative characteristics in UCCAO-operated adult mice and more comprehensively introduced a mouse model of retinal ischemia by UCCAO which can mimic the pathophysiology of ocular ischemic syndrome (OIS)
The cutting area. (b) Representative images of permanent eyelid drooping after UCCAO. (c) There was no significant change in axial length on week 2 (W2) and week 4 (W4) after UCCAO (n = 5 per group)
Summary
Retinal degeneration is a leading cause of incurable vision loss. Retinal degeneration occurs in various ways including occlusion of arteries or veins, diabetic retinopathy, or hereditary retinal diseases [1,2,3,4,5]. Ocular ischemia, occurring when the blood/oxygen supply in the eye is inadequate, commonly leads to retinal degeneration [6]. Ocular ischemia can be caused by occlusion of the ophthalmic artery, which is a branch of the internal carotid artery from the common carotid artery (CCA) [7]. Ocular ischemic syndrome (OIS) is classified as one of the vision-threatening diseases caused by occlusion of the carotid artery [6]. There is no promising treatment for OIS, and even the pathological mechanism for retinal degeneration in OIS needs fundamental investigations
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