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Inducement and Evaluation of a Murine Model of Experimental Myopia
Published on: January 22, 2019
Wnt signaling in form deprivation myopia of the mice retina
Mingming Ma1, Zhengwei Zhang1, Ergang Du2
1Department of Ophthalmology, Shanghai First People's Hospital, Shanghai Jiao Tong University, Shanghai, China; Shanghai Key Laboratory of Fundus Disease, Shanghai, China.
Background:
The canonical Wnt signaling pathway plays important roles in cellular proliferation and differentiation, axonal outgrowth, cellular maintenance in retinas. Here we test the hypothesis that elements of the Wnt signaling pathway are involved in the regulation of eye growth and prevention of myopia, in the mouse form-deprivation myopia model.
Methodology/Principal Findings:
(1) One hundred twenty-five C57BL/6 mice were randomly distributed into form-deprivation myopia and control groups. Form-deprivation myopia (FDM) was induced by suturing the right eyelid, while the control group received no treatment. After 1, 2, and 4 weeks of treatment, eyes were assessed in vivo by cycloplegic retinoscopic refraction and axial length measurement by photography or A-scan ultrasonography. Levels of retinal Wnt2b, Fzd5 and β-catenin mRNA and protein were evaluated using RT-PCR and western blotting, respectively. (2) Another 96 mice were divided into three groups: control, drugs-only, and drugs+FDM (by diffuser). Experimentally treated eyes in the last two groups received intravitreal injections of vehicle or the proteins, DKK-1 (Wnt-pathway antagonist) or Norrin (Wnt-pathway agonist), once every three days, for 4 injections total. Axial length and retinoscopic refraction were measured on the 14th day of form deprivation. Following form-deprivation for 1, 2, and 4 weeks, FDM eyes had a relatively myopic refractive error, compared with contralateral eyes. There were no significant differences in refractive error between right and left eye in control group. The amounts of Wnt2b, Fzd5 and β-catenin mRNA and protein were significantly greater in form-deprived myopia eyes than in control eyes.DKK-1 (antagonist) reduced the myopic shift in refractive error and increase in axial elongation, whereas Norrin had the opposite effect in FDM eyes.
Conclusions/Significance:
Our studies provide the first evidence that the Wnt2b signaling pathway may play a role in the development and progression of form-deprivation myopia, in a mammalian model.
Insights
The Wnt signaling pathway is implicated in myopia development. Inhibiting Wnt signaling reduced myopia progression in a mouse model, suggesting a therapeutic target for preventing myopia.
Area of Science:
- Ophthalmology
- Molecular Biology
- Genetics
Background:
- The Wnt signaling pathway regulates crucial cellular processes including proliferation and differentiation.
- This pathway is essential for axonal outgrowth and maintaining retinal cellular integrity.
Purpose of the Study:
- To investigate the role of the Wnt signaling pathway in eye growth regulation.
- To determine if Wnt signaling is involved in preventing myopia development using a mouse model.
Main Methods:
- Form-deprivation myopia (FDM) was induced in mice by eyelid suturing.
- Retinal Wnt2b, Fzd5, and β-catenin levels were measured using RT-PCR and Western blotting.
- The effects of Wnt pathway modulators (DKK-1 antagonist, Norrin agonist) on myopia were assessed.
Main Results:
- Form-deprived eyes exhibited increased myopic refractive error and axial elongation compared to controls.
- Wnt2b, Fzd5, and β-catenin expression significantly increased in FDM eyes.
- DKK-1 administration reduced myopia progression, while Norrin exacerbated it.
Conclusions:
- The Wnt2b signaling pathway is involved in the development and progression of form-deprivation myopia.
- These findings suggest Wnt signaling as a potential target for myopia control strategies.
