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Research article
Effects of hyperoxia on retinal autophagy in a mouse model of retinopathy of prematurity
Yunliang Zheng
Durg evaluation
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Purpose
To evaluate the autophagy activation of retina in an oxygen-induced retinopathy of prematurity (ROP) mouse model.
Methods
C57BL/6 mice were exposed to 75 ± 0.5% oxygen from P7 to P12, after which they were brought into room air and raised to P17. Mice underwent fluorescein angiography of the retinal vasculature on P17. The thickness and ultrastructural of retina was observed on P17. The expression of autophagy in the retina tissue was assessed by Quantitative real-time polymerase chain reaction and Western blot analysis.
Results
The neovascularization was significantly higher in the oxygen-induced mice. The retinal thickness of the oxygen-exposed group was higher than that of the control group on P17. The autophagosomes in retina of ROP mouse were observed. During the hyperoxia stage (from P8 to P13), the mRNA levels of Beclin1 (mammalian Atg6), Uncoordinated-51 like kinase 1 (ULK1), and Autophagy 5 (Atg5) were increased. At the relative hypoxia stage (raised in room air from P14 to P17), the expression of Beclin1, ULK1, and Atg5 mRNA levels was downregulated in retinas of ROP mice compare to the controls. Over time, the protein expression of Beclin-1, ULK1, and Bcl-2-associated X protein (Bax) was upregulated, but the protein expression of B-cell lymphoma 2 (Bcl-2) was downregulated.
Conclusions
Hyperoxia and relative hypoxia not only cause retinal neovascularization, but also change the autophagy markers in the retina of newborn mice.
Keywords
Retinopathy of prematurity, Autophagy, Retina, Hyperoxia
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This is a preprint. It has not completed peer review.
Research article
Effects of hyperoxia on retinal autophagy in a mouse model of retinopathy of prematurity
Yunliang Zheng
Durg evaluation
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 18 Dec, 2019
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Ophthalmology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Purpose
To evaluate the autophagy activation of retina in an oxygen-induced retinopathy of prematurity (ROP) mouse model.
Methods
C57BL/6 mice were exposed to 75 ± 0.5% oxygen from P7 to P12, after which they were brought into room air and raised to P17. Mice underwent fluorescein angiography of the retinal vasculature on P17. The thickness and ultrastructural of retina was observed on P17. The expression of autophagy in the retina tissue was assessed by Quantitative real-time polymerase chain reaction and Western blot analysis.
Results
The neovascularization was significantly higher in the oxygen-induced mice. The retinal thickness of the oxygen-exposed group was higher than that of the control group on P17. The autophagosomes in retina of ROP mouse were observed. During the hyperoxia stage (from P8 to P13), the mRNA levels of Beclin1 (mammalian Atg6), Uncoordinated-51 like kinase 1 (ULK1), and Autophagy 5 (Atg5) were increased. At the relative hypoxia stage (raised in room air from P14 to P17), the expression of Beclin1, ULK1, and Atg5 mRNA levels was downregulated in retinas of ROP mice compare to the controls. Over time, the protein expression of Beclin-1, ULK1, and Bcl-2-associated X protein (Bax) was upregulated, but the protein expression of B-cell lymphoma 2 (Bcl-2) was downregulated.
Conclusions
Hyperoxia and relative hypoxia not only cause retinal neovascularization, but also change the autophagy markers in the retina of newborn mice.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5