Author:
Zhang Xuhong,Yu Xin,Wen Yingying,Jin Le,Zhang Liyue,Zhu Hong,Zhang Dongyan,Xie Chen,Guo Dongyu,Tong Jianping,Shen Ye
Abstract
Abstract
Background
Changes in the retina and choroid blood vessels are regularly observed in myopia. However, if the retinal glial cells, which directly contact blood vessels, play a role in mammalian myopia is unknown. We aimed to explore the potential role and mechanism of retinal glial cells in form deprived myopia.
Methods
We adapted the mice form-deprivation myopia model by covering the right eye and left the left eye open for control, measured the ocular structure with anterior segment optical coherence tomography, evaluated changes in the morphology and distribution of retinal glial cells by fluorescence staining and western blotting; we also searched the online GEO databases to obtain relative gene lists and confirmed them in the form-deprivation myopia mouse retina at mRNA and protein level.
Results
Compared with the open eye, the ocular axial length (3.54 ± 0.006 mm v.s. 3.48 ± 0.004 mm, p = 0.027) and vitreous chamber depth (3.07 ± 0.005 mm v.s. 2.98 ± 0.006 mm, p = 0.007) in the covered eye became longer. Both glial fibrillary acidic protein and excitatory amino acid transporters 4 elevated. There were 12 common pathways in human myopia and anoxic astrocytes. The key proteins were also highly relevant to atropine target proteins. In mice, two common pathways were found in myopia and anoxic Müller cells. Seven main genes and four key proteins were significantly changed in the mice form-deprivation myopia retinas.
Conclusion
Retinal astrocytes and Müller cells were activated in myopia. They may response to stimuli and secretory acting factors, and might be a valid target for atropine.
Funder
The Natural Science Foundation of Zhejiang Province
The Key Research and Development Program of Zhejiang Province
The Strategic Priority Research Program of Chinese Academy of Sciences
Publisher
Springer Science and Business Media LLC
Subject
Ophthalmology,General Medicine
Cited by
6 articles.
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