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Author Spotlight: Advancing Corneal Innervation Research Through Innovative Models
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AQP5 Regulates Corneal Nerve Distribution Through NETRIN-1 and SLIT3.
Wenshuo Han1, Yaning Liu1, Peirong Song1
1School of Basic Medicine, Qingdao University, Qingdao, Shandong, China.
Investigative Ophthalmology & Visual Science
|November 4, 2025
Summary
Aquaporin 5 (AQP5) deficiency impairs corneal nerve structure by altering the JUN-D-Ntn1/Slit3 pathway, suggesting AQP5 as a therapeutic target for neurotrophic keratopathy (NK).
Area of Science:
- Ophthalmology
- Neuroscience
- Molecular Biology
Background:
- Neurotrophic keratopathy (NK) involves abnormal corneal nerves.
- Aquaporin 5 (AQP5) is a water channel protein.
- The precise role of AQP5 in corneal innervation is not fully understood.
Purpose of the Study:
- To investigate the role of AQP5 in corneal nerve distribution.
- To explore the regulation of corneal nerves by AQP5 through the JUN-D-Ntn1/Slit3 signaling pathway.
Main Methods:
- Comparison of corneal nerve density in wild-type and Aqp5 knockout mice using immunolabeling.
- In vitro coculture of trigeminal ganglion neurons with NETRIN-1 or SLIT3.
- Assessment of JUN-D binding to Ntn1 and Slit3 promoters via ChIP-PCR.
- Evaluation of corneal epithelial healing and nerve regeneration after scraping, with JUN-D modulation.
Main Results:
- Aqp5 knockout mice exhibited reduced corneal nerve density.
- NETRIN-1 levels were decreased, and SLIT3 levels increased in Aqp5 knockout corneas.
- NETRIN-1 promoted axonal growth, while SLIT3 inhibited it.
- JUN-D modulation affected corneal epithelial healing and nerve regeneration.
Conclusions:
- AQP5 deficiency disrupts corneal nerve architecture, potentially contributing to NK.
- AQP5 regulates corneal nerve distribution via the JUN-D-Ntn1/Slit3 pathway.
- This pathway presents potential therapeutic targets for NK treatment.
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