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MYRF as an Entry Point to Study Mesothelium Function in Lung Development and Injury Repair

Award Number: R01HL172027
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 02/01/2024
PERIOD OF PERFORMANCE END DATE: 12/31/2027

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MYRF as an Entry Point to Study Mesothelium Function in Lung Development and Injury Repair - PROJECT SUMMARY/ABSTRACT The mesothelium is an overlooked cell type that is also ubiquitous: it is the most external cell layer that encapsulates all internal organs and lines the body cavities. The best-known canonical function of the mesothelium is to produce lubricant to facilitate organ sliding past each other and the body wall. The mesothelium is composed of a single layer of large and flat squamous epithelial cells that is derived from the mesoderm lineage. In the lung, aside from being the site of asbestos-induced mesothelioma, the role of this fundamental cell layer in lung development and injury repair is poorly understood, and is the focus of this study. Our entry point to studying the mesothelium is Myelin Regulatory Factor (MYRF), a transcription factor. Variants in the MYRF gene have been identified in congenital diaphragmatic hernia (CDH) patients. CDH carries a high mortality rate at birth largely due to respiratory distress. In the lung, MYRF is expressed in the mesothelial cells and alveolar type I cells, two large and flat cell types of the mesenchyme and epithelium, respectively. In mice, while inactivation of Myrf in the lung epithelium led to no discernable phenotypes, inactivation of Myrf in the mesenchyme led to a clear CDH phenotype, including organ herniation, lung hypoplasia and lethality at birth. Later inactivation of Myrf bypassed embryonic lethality, revealing a striking subpleural fibrosis phenotype in the postnatal lung. In the adult, bleomycin treatment of these mutant lungs led to exaggerated injury compared to control, implicating subpleural myofibroblasts as a possible contributor to fibrosis progression. In this study, we will use MYRF as an entry point to investigate mesothelium function as a signaling center in lung growth (Aim 1), as an active barrier in homeostasis (Aim 2), and as an instigator of pathogenesis in lung repair (Aim 3). Our findings will delineate the fundamental role of the mesothelium and its quintessential transcription driver MYRF in lung development, homeostasis, injury and repair.


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 = $542,285 )
2026	2026	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Lung Diseases Research	000	3	1/31/2026	NON-COMPETING CONTINUATION	$542,285
														Subtotal = $542,285

Issue Date FY: 2025 ( Subtotal = $570,826 )
2025	2025	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Lung Diseases Research	000	2	12/30/2024	NON-COMPETING CONTINUATION	$513,744
2025	2025	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Lung Diseases Research	001	2	8/27/2025	NON-COMPETING CONTINUATION	$57,082
														Subtotal = $570,826

Issue Date FY: 2024 ( Subtotal = $570,826 )
2024	2024	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Lung Diseases Research	000	1	1/26/2024	NEW	$513,744
2024	2024	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Lung Diseases Research	001	1	6/29/2024	NEW	$57,082
														Subtotal = $570,826

Grand Total All Awards = $1,683,937

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MYRF as an Entry Point to Study Mesothelium Function in Lung Development and Injury Repair

Award Number: R01HL172027

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 02/01/2024

PERIOD OF PERFORMANCE END DATE: 12/31/2027

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