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GSDMD deficiency ameliorates hyperoxia-induced BPD and ROP in neonatal mice
Sarah Sonny1, Huijun Yuan1, Shaoyi Chen1
1Neonatology and Batchelor Children Research Institute, University of Miami Miller School of Medicine, 1580 NW 10thAve, Miami, FL, 33136, USA.
Scientific Reports
|January 4, 2023
Summary
Gasdermin D (GSDMD) plays a key role in hyperoxia-induced bronchopulmonary dysplasia and retinopathy of prematurity in premature infants. Targeting GSDMD may offer new treatments for these conditions.
Area of Science:
- Neonatal Medicine
- Inflammation and Immunology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are significant complications in premature infants treated with oxygen.
- A mechanistic link between hyperoxia, BPD, and ROP is not fully understood.
- Gasdermin D (GSDMD) is a critical mediator of pyroptosis and inflammation.
Purpose of the Study:
- To investigate the role of GSDMD in the pathogenesis of hyperoxia-induced BPD and ROP.
- To define the mechanistic pathways involving GSDMD in these conditions.
Main Methods:
- Utilized global GSDMD knockout (GSDMD-KO) mouse models.
- Exposed mice to hyperoxia to induce BPD and ROP.
- Performed histological, molecular, and RNA sequencing analyses on lung and retinal tissues.
Main Results:
- GSDMD-KO significantly protected against hyperoxia-induced BPD and ROP.
- GSDMD deficiency reduced inflammation, cell death, and improved tissue development in lungs and retinas.
- Shared inflammatory and developmental pathways were identified in both conditions and modulated by GSDMD-KO.
Conclusions:
- GSDMD is crucial in the development of hyperoxia-induced BPD and ROP.
- Targeting GSDMD presents a potential therapeutic strategy for preventing and treating BPD and ROP in premature infants.
