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Defining a new model of evaporative dry eye disease

Award Number: R21EY037056
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 05/01/2025
PERIOD OF PERFORMANCE END DATE: 06/16/2025

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Defining a new model of evaporative dry eye disease - PROJECT SUMMARY Dry eye disease (DED) is a multifactorial ophthalmic disorder with many underlying causes unified by the presence of an abnormal tear film that leads to inflammation and irritation of the ocular surface. If left untreated, DED can lead to corneal fibrosis, neovascularization and impaired vision. DED is further classified as either aqueous deficient dry eye or evaporative dry eye disease (EDED) based on the suspected etiopathogenesis, with EDED representing 87% of total DED cases. Despite the frequency of EDED in the population, there is no consensus animal model for studying the pathogenesis of EDED and to test novel therapeutics. Recently, we have utilized an emerging murine model of EDED, a mutant mouse lacking the acyl- CoA wax alcohol acyltransferase 2 (Awat2) gene that encodes a key enzyme responsible for the synthesis of long chain wax esters from the meibomian glands, a critical group of lipids in the tear film. The Awat2 knockout (KO) mice have a lackluster tear film that contains white concretions, which appear to be the altered meibomian gland lipids. This abnormal composition of the tear film lipids leads to destabilization of the tear film and exposure of the underlying corneal surface. Therefore, the Awat2 KO mice develop ocular surface disease secondary to an underlying dysfunction in lipid synthesis, similar to patients with EDED. Preliminary data from our laboratory suggest that Awat2 KO mice have functional and molecular alterations to the ocular surface that are consistent with phenotype of human EDED. We hypothesize that a dysregulated tear film lipid layer leads to (1) damage to the topographic features of the corneal surface that help to adhere the tear film to the cornea, and (2) breakdown of the corneal epithelial barrier function. These pathological changes result in the chronic cycle of inflammation and irritation that human patients with EDED experience. In this proposal, we will (1) define the clinical, topographical and ultrastructural abnormalities of the ocular surface in Awat2 KO mice and (2) determine the impact of EDED on the corneal epithelial barrier function. Ultimately, we aim to identify the age of onset and progression of ocular surface disease in the Awat2 mice to guide future studies investigating the pathogenesis of EDED and to test novel therapeutic interventions.


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 = -$442,750 )
2026	2025	UNIVERSITY OF CALIFORNIA, DAVIS	1850 RESEARCH PARK DR STE 300	DAVIS	CA	95618	YOLO	USA	Vision Research	000	1	12/19/2025	NEW	-$442,750
														Subtotal = -$442,750

Issue Date FY: 2025 ( Subtotal = $442,750 )
2025	2025	UNIVERSITY OF CALIFORNIA, DAVIS	1850 RESEARCH PARK DR STE 300	DAVIS	CA	95618	YOLO	USA	Vision Research	000	1	4/25/2025	NEW	$442,750
														Subtotal = $442,750

Grand Total All Awards = $0

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Defining a new model of evaporative dry eye disease

Award Number: R21EY037056

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 05/01/2025

PERIOD OF PERFORMANCE END DATE: 06/16/2025

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