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Inducement and Evaluation of a Murine Model of Experimental Myopia
Published on: January 22, 2019
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Dysfunction of VIPR2 leads to myopia in humans and mice
Fuxin Zhao1,2, Qihang Li1,2, Wei Chen3,4
1School of Optometry and Ophthalmology and Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Journal of Medical Genetics
|December 15, 2020
Summary
The VIP-VIPR2 signaling pathway influences myopia development in mice. Targeting this pathway could offer new strategies for controlling myopia progression.
Area of Science:
- Ophthalmology
- Neuroscience
- Genetics
Background:
- Myopia is a leading cause of refractive error with poorly understood pathogenesis.
- The role of the retinal VIP-VIPR2 signaling pathway in myopia development requires investigation.
Purpose of the Study:
- To determine if the VIP-VIPR2 signaling pathway axis affects myopia development in mice.
- To investigate the functional role of VIPR2 in refractive development.
Main Methods:
- Association analysis meta-study and transcriptomic analyses (single-cell and bulk RNA sequencing).
- Pharmacological manipulation of VIPR2 and VIPR2 gene knockout studies in mice.
- Assessment of refractive development and retinal function.
Main Results:
- A SNP in the VIPR2 gene associated with high myopia in a Chinese Han cohort.
- Form deprivation downregulated retinal VIP mRNA and inhibited cAMP signaling in VIPR2+ cells.
- VIPR2 antagonist induced myopia, agonist inhibited it, and VIPR2 knockout mice showed myopia and altered bipolar cell activity.
Conclusions:
- VIPR2 dysfunction impairs bipolar cell function, affecting signal transduction and electrical activity.
- The VIP-VIPR2 signaling pathway is a potential novel target for controlling myopia development.
- Findings suggest a link between VIPR2 function and form deprivation myopia (FDM).
