4.7 Article

Hyperoxia induces alveolar epithelial cell apoptosis by regulating mitochondrial function through small mothers against decapentaplegic 3 (SMAD3) and extracellular signal-regulated kinase 1/2 (ERK1/2)

期刊

BIOENGINEERED
卷 13, 期 1, 页码 242-252

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2021.2012953

关键词

Hyperoxia; mitochondrial function; cell apoptosis; alveolar epithelial cells; lung damage; neonatal lung dysfunction

资金

  1. National Natural Science Foundation of China [81560256]

向作者/读者索取更多资源

Oxygen therapy and mechanical ventilation are commonly used methods to treat critically ill newborns, but they often lead to adverse effects such as chronic lung disease. This study established an in vitro model to investigate the molecular basis of hyperoxia-induced lung damage in type II alveolar epithelial cells (AECIIs). The results showed that SMAD/ERK signaling plays a critical role in regulating AECII behavior in different oxygen environments.
Oxygen therapy and mechanical ventilation are widely used to treat and manage neonatal emergencies in critically ill newborns. However, they are often associated with adverse effects and result in conditions such as chronic lung disease and bronchopulmonary dysplasia. Hence, aclear understanding of the mechanisms underlying hyperoxia-induced lung damage is crucial in order to mitigate the side effects of oxygen-based therapy. Here, we have established an in vitro model of hyperoxia-induced lung damage in type II alveolar epithelial cells (AECIIs) and delineated the molecular basis of oxygen therapy-induced impaired alveolar development. Thus, AECIIs were exposed to a hyperoxic environment and their cell viability, cell cycle progression, apoptosis, mitochondrial integrity and dynamics, and energy metabolism were assessed. The results showed that hyperoxia has no significant effect as an inhibitor of SMAD3 and ERK1/2 in AECIIs, but leads to significant inhibition of cell viability. Further, hyperoxia was found to promote AECII apoptosis and mitochondrial, whereas chemical inhibition of SMAD3 or ERK1/2 further exacerbated the detrimental effects of hyperoxia in AECIIs. Overall, these findings presented herein demonstrate the critical role of SMAD/ERK signaling in the regulation of AECII behavior in varying oxygen environments. Thus, this study offers novel insights for the prevention of neonatal lung dysfunction in premature infants.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据