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Changes in transient receptor potential melastatin 8 expression and function after corneal nerve regeneration

Award Number: F30EY038057
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2030

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Changes in transient receptor potential melastatin 8 expression and function after corneal nerve regeneration - PROJECT SUMMARY/ABSTRACT Corneal nerves consist of the densest network of innervation in the body, branching from the trigeminal ganglion (TG) and terminating at the corneal epithelial surface. These nerve endings express ion channel receptors that regulate essential sensory functions such as cooling, hydration, nociception, and mechanosensation. The transient receptor potential melastatin 8 (TRPM8), known as the cold thermoreceptor, is a crucial ion channel that maintains corneal homeostasis via blink reflex, tear response, and supply of trophic factors upon cold stimulus. Thus, intact corneal nerve innervation is crucial for sensory functions and overall corneal health. However, corneal nerve injuries resulting from trauma, surgery, or disease often lead to incomplete or maladaptive nerve regeneration, which subsequently affects the function of sensory modalities such as TRPM8. Dysfunction of sensory modalities can lead to neuropathic pain, impaired sensation, and poor wound healing, significantly impacting vision and quality of life. Although TRPM8 has a known role in corneal epithelial and nerve health, changes in overall corneal nerve structure, TRPM8 expression, and TRPM8 function during and after nerve regeneration remain poorly understood. This project aims to determine how TRPM8 is affected by injury, how it contributes to corneal nerve recovery, and its potential as a therapeutic target. The injury model for this project is corneal epithelial debridement (CED) in rodent models. It will mimic clinical contexts like corneal abrasion, laser-assisted in situ keratomileusis (LASIK), and other refractive surgeries. The first objective of this proposal will investigate the anatomical and molecular recovery of TRPM8-expressing nerves using immunohistochemistry and 3-D light sheet microscopy (LSM) of TRPM8 protein expression. Spatial transcriptomics of TGs will also be employed to correlate potential regulatory changes at the transcriptional level with changes in TRPM8 protein expression. The second objective will assess the effect of TRPM8 deletion on corneal nerve regeneration and how TRPM8 modulates nerve repair and epithelial integrity. The final objective of this proposal will utilize in vivo electrophysiology and functional behavioral assays to evaluate TRPM8 functional activity following CED and the application of TRPM8 agonists, menthol and icilin, at acute and chronic time points. Overall, this research addresses a critical gap in understanding the mechanisms that direct corneal nerve recovery and provides insight into developing targeted therapies that could improve outcomes for patients suffering from nerve-related ocular pathologies.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $55,114 )
2026	2026	UNIVERSITY OF ILLINOIS	809 S MARSHFIELD AVE M/C 551	CHICAGO	IL	60612	COOK	USA	Vision Research	000	1	6/11/2026	NEW	$55,114
2026	2026	UNIVERSITY OF ILLINOIS	809 S MARSHFIELD AVE M/C 551	CHICAGO	IL	60612	COOK	USA	Vision Research	001	1	6/11/2026	NEW	$0
														Subtotal = $55,114

Grand Total All Awards = $55,114

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Changes in transient receptor potential melastatin 8 expression and function after corneal nerve regeneration

Award Number: F30EY038057

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2030

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