Deletion Of S100A16 Protein In Mice Causes Respiratory Failure And Death At Birth

Background:Epithelial cells lining the peripheral lung synthesize pulmonary surfactant that reduces surface tension at the air-liquid interface.Lack of surfactant lipids and proteins in the lungs causes respiratory distress syndrome,a common cause of morbidity and mortality in preterm infants.Here,we generate S100A16 knock-out mice and demonstrate that loss of the S100A16 gene causes neonatal lethality at birth.We show that S100A16 plays a crucial role in the maturation of the respiratory epithelium in late gestation,being required for the production of surfactant lipids and proteins necessary for lung functionMethods:After the construction of transgenic mice models,we used HE staining method(hematoxylin and eosin staining,HE)to observe the lungs of different phenotypes in mice,and Western blotting to study the expression of surfactant protein in the lungs.To investigate the mechanism of the effect of S100A16 on the expression of surfactant protein.Results:Examination reveals that maturation of lung in the homozygous mutants is delayed,as indicated by narrowed air spaces,thickened interstitial septa.Deletion of the S100A16 gene in respiratory epithelial cells in fetal mice caused respiratory failure at birth.Collectively,this study uncovers an important role of S100A16 for lung maturation and neonatal survival.Discovery of the role of S100A16 in lung maturation helps to understand the molecular regulation in lung development.Conclusion:S100A16 is required for alveolar epithelium maturation and function.S100A16 deletion causes fetal lung immaturity and neonatal death with altered expression of genes important for lung development.