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Bronchopulmonary dysplasia (BPD) is characterized by a severe impairment in lung alveolarization and vascular development. We have previously shown that pulmonary angiogenesis is preserved in hyperoxia-exposed female mice accompanied by increased  miR-30a  expression, which is a proangiogenic miRNA. Also,  miR-30a  expression is decreased in human BPD. HIF-1 α  plays an essential role in postnatal lung development, especially in recovery from hyperoxic injury.  Snai1  activation promotes pathological fibrosis through many mechanisms including Endo-MT, which may in turn adversely impact lung vascular development. Our objective was to test the hypothesis that higher miR-30a expression through  HIF-1α  decreases  Snai1  expression in females and attenuates injury in the developing lung. Neonatal male and female mice (C57BL/6) were exposed to hyperoxia (P1-5, 0.95 FiO 2 ) and euthanized on P21. Neonatal human pulmonary microvascular endothelial cells (HPMECs; 18-24-week gestation donors; 3/group either sex) were subjected to hyperoxia (95% O 2  and 5% CO 2 ) or normoxia (air and 5% CO 2 ) up to 72 h.  Snai1  expression was measured in HPMECs  in vitro  and in neonatal mouse lungs  in vivo . Also,  Snai1  expression was measured in HPMECs after  miR-30a  mimic and  miR-30a  inhibitor treatment. To further establish the potential regulation of  miR-30a  by  Hif-1α ,  miR-30a  expression after Hif-1 α  inhibition was measured in HPMECs.  In vivo ,  Snai1  expression was decreased in neonatal female lungs compared to males at P7. Increased  Snai1  expression was seen in male HPMECs upon exposure to hyperoxia  in vitro . Treatment with the  miR-30a  mimic decreased  Snai1  expression in HPMECs, while  miR-30a inhibition  significantly increased  Snai1  expression in HPMECs. siRNA-mediated loss of  Hif-1α  expression in HPMECs decreased  miR-30a expression .  Hif-1α  may lead to differential sex-specific miR-30a expression and may contribute to protection from hyperoxic lung injury in female neonatal mice through decreased  Snai1  expression.

Role of HIF-1α-miR30a-Snai1 Axis in Neonatal Hyperoxic Lung Injury