PMID- 37987780
OWN - NLM
STAT- MEDLINE
DCOM- 20240105
LR  - 20240208
IS  - 1522-1504 (Electronic)
IS  - 1040-0605 (Linking)
VI  - 326
IP  - 1
DP  - 2024 Jan 1
TI  - Exogenous hydrogen sulfide attenuates hyperoxia effects on neonatal mouse 
      airways.
PG  - L52-L64
LID - 10.1152/ajplung.00196.2023 [doi]
AB  - Supplemental O(2) remains a necessary intervention for many premature infants 
      (<34 wk gestation). Even moderate hyperoxia (<60% O(2)) poses a risk for 
      subsequent airway disease, thereby predisposing premature infants to pediatric 
      asthma involving chronic inflammation, airway hyperresponsiveness (AHR), airway 
      remodeling, and airflow obstruction. Moderate hyperoxia promotes AHR via effects 
      on airway smooth muscle (ASM), a cell type that also contributes to impaired 
      bronchodilation and remodeling (proliferation, altered extracellular matrix). 
      Understanding mechanisms by which O(2) initiates long-term airway changes in 
      prematurity is critical for therapeutic advancements for wheezing disorders and 
      asthma in babies and children. Immature or dysfunctional antioxidant systems in 
      the underdeveloped lungs of premature infants thereby heightens susceptibility to 
      oxidative stress from O(2). The novel gasotransmitter hydrogen sulfide (H(2)S) is 
      involved in antioxidant defense and has vasodilatory effects with oxidative 
      stress. We previously showed that exogenous H(2)S exhibits bronchodilatory 
      effects in human developing airway in the context of hyperoxia exposure. Here, we 
      proposed that exogenous H(2)S would attenuate effects of O(2) on airway 
      contractility, thickness, and remodeling in mice exposed to hyperoxia during the 
      neonatal period. Using functional [flexiVent; precision-cut lung slices (PCLS)] 
      and structural (histology; immunofluorescence) analyses, we show that H(2)S 
      donors mitigate the effects of O(2) on developing airway structure and function, 
      with moderate O(2) and H(2)S effects on developing mouse airways showing a sex 
      difference. Our study demonstrates the potential applicability of low-dose H(2)S 
      toward alleviating the detrimental effects of hyperoxia on the premature lung.NEW 
      & NOTEWORTHY Chronic airway disease is a short- and long-term consequence of 
      premature birth. Understanding effects of O(2) exposure during the perinatal 
      period is key to identify targetable mechanisms that initiate and sustain adverse 
      airway changes. Our findings show a beneficial effect of exogenous H(2)S on 
      developing mouse airway structure and function with notable sex differences. 
      H(2)S donors alleviate effects of O(2) on airway hyperreactivity, contractility, 
      airway smooth muscle thickness, and extracellular matrix deposition.
FAU - Bartman, Colleen M
AU  - Bartman CM
AUID- ORCID: 0000-0002-3624-669X
AD  - Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, 
      Minnesota, United States.
FAU - Schiliro, Marta
AU  - Schiliro M
AD  - Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, 
      Minnesota, United States.
AD  - Department of Anesthesiology and Critical Care Medicine, School of Medicine and 
      Surgery, University of Milano-Bicocca, Monza, Italy.
FAU - Nesbitt, Lisa
AU  - Nesbitt L
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, 
      Minnesota, United States.
FAU - Lee, Kenge K
AU  - Lee KK
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, 
      Minnesota, United States.
FAU - Prakash, Y S
AU  - Prakash YS
AUID- ORCID: 0000-0002-2968-224X
AD  - Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, 
      Minnesota, United States.
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, 
      Minnesota, United States.
FAU - Pabelick, Christina M
AU  - Pabelick CM
AUID- ORCID: 0000-0002-4632-2174
AD  - Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, 
      Minnesota, United States.
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, 
      Minnesota, United States.
LA  - eng
GR  - 20POST35210002/American Heart Association (AHA)/
GR  - R01HL160570/HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/
GR  - R01HL056470/HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20231121
PL  - United States
TA  - Am J Physiol Lung Cell Mol Physiol
JT  - American journal of physiology. Lung cellular and molecular physiology
JID - 100901229
RN  - YY9FVM7NSN (Hydrogen Sulfide)
RN  - 0 (Antioxidants)
SB  - IM
MH  - Humans
MH  - Pregnancy
MH  - Child
MH  - Animals
MH  - Female
MH  - Mice
MH  - Male
MH  - *Hyperoxia/metabolism
MH  - Animals, Newborn
MH  - *Hydrogen Sulfide/pharmacology
MH  - Antioxidants/pharmacology
MH  - Lung/metabolism
MH  - *Asthma/pathology
OTO - NOTNLM
OT  - airway hyperresponsiveness
OT  - airway smooth muscle
OT  - asthma
OT  - hyperoxia
OT  - prematurity
EDAT- 2023/11/21 12:44
MHDA- 2024/01/05 06:42
CRDT- 2023/11/21 11:05
PHST- 2024/01/05 06:42 [medline]
PHST- 2023/11/21 12:44 [pubmed]
PHST- 2023/11/21 11:05 [entrez]
AID - 10.1152/ajplung.00196.2023 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2024 Jan 1;326(1):L52-L64. doi: 
      10.1152/ajplung.00196.2023. Epub 2023 Nov 21.