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Interactions of MG53 and GsdmD for Neutrophil Pyroptosis Inhibition

Award Number: R16GM153571
ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/01/2025
PERIOD OF PERFORMANCE END DATE: 05/31/2029

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Interactions of MG53 and GsdmD for Neutrophil Pyroptosis Inhibition - Project Summary/Abstract The proposed research project aims to understand how MG53, a membrane repair protein, protects heart cells after myocardial infarction (MI). When MI occurs, it causes inflammation and damage to heart cells, which can lead to further complications if not controlled. The project focuses on a process called pyroptosis, which is a type of cell death that contributes to inflammation. MG53 is known to help repair damaged cell membranes, while another protein, GsdmD, forms holes in cell membranes, leading to membrane rupture and subsequent cell death. The central hypothesis is that MG53 may prevent this harmful process by interacting with GsdmD in neutrophil cells. The long-term goal is to find a way to fine-tune the immune response to promote healing after MI without causing excessive inflammation. Preliminary data suggest that (1) Pyroptosis plays a key role in the inflammatory response shortly after MI. (2) MG53 reduces GsdmD activation and pyroptosis and improves heart damage after MI. (3) Activated GsdmD is found in neutrophils after MI. Since MG53 is naturally present in the body, targeting it for therapy should be safe and not trigger an immune reaction. The hypothesis is that MG53 prevents pyroptosis by interacting with GsdmD in neutrophils, stopping GsdmD from activating or blocking the holes activated GsdmD creates. The research will have two main Specific Aims. Aim 1: To study how MG53 and GsdmD interact before and after GsdmD activation. Research design and method: Aim 1 will investigate the binding of MG53 and GsdmD in solution and MG53’s and activated GsdmD’s colocalization on liposomes. Aim 1 will also employ an MG53 mutant that lacks membrane repair function to elucidate MG53’s role in protecting neutrophils after pyroptosis. Aim 2: To determine if neutrophil pyroptosis contributes to heart cell death. Research design and method: Aim 2 will assess the contribution of neutrophil pyroptosis to post-MI cardiomyocyte death by utilizing neutrophil- specific GsdmD knockout mice for post-MI evaluation and by evaluating if recombinant MG53 can protect cardiomyocytes from neutrophil pyroptosis. This research could lead to new therapies for treating MI by reducing damage and promoting healing.


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 = $155,463 )
2026	2026	ST JOHN'S UNIVERSITY, NEW YORK	8000 UTOPIA PKWY	JAMAICA	NY	11439	QUEENS	USA	Biomedical Research and Research Training	000	2	5/1/2026	NON-COMPETING CONTINUATION	$155,463
														Subtotal = $155,463

Issue Date FY: 2025 ( Subtotal = $155,463 )
2025	2025	ST JOHN'S UNIVERSITY, NEW YORK	8000 UTOPIA PKWY	JAMAICA	NY	11439	QUEENS	USA	Biomedical Research and Research Training	000	1	8/29/2025	NEW	$155,463
														Subtotal = $155,463

Grand Total All Awards = $310,926

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Interactions of MG53 and GsdmD for Neutrophil Pyroptosis Inhibition

Award Number: R16GM153571

ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 09/01/2025

PERIOD OF PERFORMANCE END DATE: 05/31/2029

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