Maternal Vitamin D deficiency induces transcriptomic changes in newborn rat lungs
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Vitamin D deficiency during pregnancy is common and is related to several maternal and fetal morbidities. Past studies suggest that vitamin D plays a role in normal lung development and we have shown that vitamin D regulates lung alveolar and vascular growth and preserves lung structure in experimental bronchopulmonary dysplasia (BPD) through improved pro-angiogeneic signaling. In addition, maternal vitamin D deficiency causes abnormal airway, alveolar, and vascular growth, as well as impaired lung function and airway hyper-reactivity in newborn rats. However, the mechanisms responsible for these physiologic effects are unknown. To gain insight into the role that maternal vitamin D status has on fetal lung development we used an unbiased transcriptomic approach to identify pathways altered in the lungs of offspring from vitamin D deficient dams.
妊娠期维生素D缺乏较为常见,且与多种母体及胎儿并发症相关。既往研究表明,维生素D参与正常肺发育进程;本团队此前已证实,在实验性支气管肺发育不良(bronchopulmonary dysplasia, BPD)模型中,维生素D可通过增强促血管生成信号通路,调控肺肺泡与血管生长,并维持肺组织结构完整。此外,母体维生素D缺乏可导致新生大鼠气道、肺泡及血管生长异常,同时伴随肺功能受损与气道高反应性。然而,介导上述生理效应的具体分子机制尚未明确。为深入探究母体维生素D状态对胎儿肺发育的调控作用,本研究采用无偏转录组学方法(unbiased transcriptomic approach),筛选维生素D缺乏孕鼠子代肺组织中表达异常的信号通路。



