Regulation of Oxidative Stress by Nitric Oxide Defines Lung Development and Diseases

Abstract

Development and maturation of the lung airways primarily take place in two different phases: first during embryonic days and second during postnatal days. During postnatal development, rapid angiogenesis and alveolarization are necessary to attain the capacity of the lung to support the need of the baby. During lung development, alteration in ROS level may significantly compromise maturation of the alveolar structure. We have employed a unique approach to achieve alteration in ROS level in the chick embryos to ascertain ROS function in early lung development. We have used a known ROS quenching nitric oxide (NO) donor and a ROS inducer called thalidomide, a known teratogen. Using next-generation high-throughput sequencing (NGS) analysis, we have performed the transcriptomic analysis of the NO- and thalidomide-treated chick embryos. Using STRING database, we have identified a set of lung-associated developmental genes that were significantly altered upon NO and/or thalidomide treatment and thus providing evidence that interplaying with cellular ROS level could possible alter the set of genes involved in early lung development. In conclusion, the current study shed light that alteration of ROS level could modulate the expression of early genes which are required for normal lung development and maturation.