Immunohistochemical analysis of apoptosis and cell proliferation in lungs of
            premature infants with chronic lung disease (bronchopulmonary dysplasia)

Witkowski, Sandra Mara; Noronha, Lúcia de; Okamoto, Cristina Terumy; Neto, Carlos F. Oldenburg; Almeida, Tammy; Nagashima, Seigo; Bahr, João Augusto

doi:10.5935/1676-2444.20160064

Cited by 1 publication

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“…The high levels of ROS upon hyperoxia can overwhelm the antioxidant systems in pulmonary cell types, which then become targets of ROS-induced injury and death. Studies show that hyperoxia-induced lung injury is associated with the death of alveolar epithelial cells, showing features of both apoptosis and necrosis ( Das et al, 2004 ; Tong et al, 2021 ; Witkowski et al, 2016 ). Preterm human neonates who have received mechanical ventilation show higher levels of apoptosis, particularly, in epithelial cells ( Lukkarinen et al, 2003 ).…”

Section: Lung Development and Bpdmentioning

confidence: 99%

Hyperoxia-induced bronchopulmonary dysplasia: better models for better therapies

Giusto

Wanczyk

Jensen

et al. 2021

Disease Models &Amp; Mechanisms

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Bronchopulmonary dysplasia (BPD) is a chronic lung disease caused by exposure to high levels of oxygen (hyperoxia) and is the most common complication that affects preterm newborns. At present, there is no cure for BPD. Infants can recover from BPD; however, they will suffer from significant morbidity into adulthood in the form of neurodevelopmental impairment, asthma and emphysematous changes of the lung. The development of hyperoxia-induced lung injury models in small and large animals to test potential treatments for BPD has shown some success, yet a lack of standardization in approaches and methods makes clinical translation difficult. In vitro models have also been developed to investigate the molecular pathways altered during BPD and to address the pitfalls associated with animal models. Preclinical studies have investigated the efficacy of stem cell-based therapies to improve lung morphology after damage. However, variability regarding the type of animal model and duration of hyperoxia to elicit damage exists in the literature. These models should be further developed and standardized, to cover the degree and duration of hyperoxia, type of animal model, and lung injury endpoint, to improve their translational relevance. The purpose of this Review is to highlight concerns associated with current animal models of hyperoxia-induced BPD and to show the potential of in vitro models to complement in vivo studies in the significant improvement to our understanding of BPD pathogenesis and treatment. The status of current stem cell therapies for treatment of BPD is also discussed. We offer suggestions to optimize models and therapeutic modalities for treatment of hyperoxia-induced lung damage in order to advance the standardization of procedures for clinical translation.

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