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Abstract
Moderate hyperoxia (30%–60% O2) in premature infants promotes bronchial airway hyperresponsiveness (AHR) via airway smooth muscle (ASM), a key regulator of bronchoconstriction, bronchodilation, and remodeling. Understanding how O2 exposure drives long-term bronchial changes in prematurity is critical for developing therapies for airway disease across the lifespan. Premature lungs have immature antioxidant defenses, potentially due to disrupted mitochondrial dynamics, increasing susceptibility to O2-induced oxidative stress. Thus, mitochondrial homeostasis is highly relevant to ASM dysfunction and airway disease. We propose that hyperoxia in prematurity promotes mitochondrial dysfunction, and that the gasotransmitter hydrogen sulfide (H2S) mitigates O2-induced mitochondrial damage in developing ASM. Human fetal ASM (fASM) cells were exposed to moderate hyperoxia to investigate the effects of exogenous H2S donors (GYY4137, AP39) and stabilization of cystathionine β-synthase (CBS), an H2S biosynthetic enzyme, on mitochondrial structure and function. Hyperoxia impaired fASM cell mitochondrial integrity, while H2S donors in particular, or CBS stabilization attenuated adverse O2 effects on mitochondrial morphology, ROS, respiration, calcium regulation, and contractility. These findings highlight the therapeutic potential of H2S in the premature lung exposed to moderate hyperoxia.
Authors
Colleen M. Bartman, Michael Thompson, Samantha K. Hamrick, Niyati A. Borkar, Daniel Pfeffer-Kleemann, Preetham Ravi, Marta Schiliro, Yak Nak, Christian Vivar Ramon, Li Drake, Y.S. Prakash, Christina Pabelick
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