Chen Xueyu, Zhong Junyan, Han Dongshan, Yao Fang, Zhao Jie, Wagenaar Gerry T M, Yang Chuanzhong, Walther Frans J
Laboratory of Neonatology, Department of Neonatology, Affiliated Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, China.
Department of Neonatology, Shenzhen Maternity and Child Healthcare Hospital, The First School of Clinical Medicine, Southern Medical University, Shenzhen, China.
Front Pediatr. 2021 May 7;9:625031. doi: 10.3389/fped.2021.625031. eCollection 2021.
Bronchopulmonary dysplasia (BPD) is a neonatal chronic lung disease characterized by an arrest in alveolar and vascular development. BPD is secondary to lung immaturity, ventilator-induced lung injury, and exposure to hyperoxia in extremely premature infants, leading to a lifelong impairment of lung function. Recent studies indicate that the lung plays an important role in platelet biogenesis. However, the dynamic change of platelet production during lung development and BPD pathogenesis remains to be elucidated. We investigated the dynamic change of platelet parameters in extremely premature infants during BPD development, and in newborn rats during their normal development from birth to adulthood. We further studied the effect of hyperoxia exposure on platelet production and concomitant pulmonary maldevelopment in an experimental BPD rat model induced by prolonged exposure to hyperoxia. We detected a physiological increase in platelet count from birth to 36 weeks postmenstrual age in extremely premature infants, but platelet counts in extremely premature infants who developed BPD were persistently lower than gestational age-matched controls. In line with clinical findings, exposure to hyperoxia significantly decreased the platelet count in neonatal rats. Lung morphometry analysis demonstrated that platelet counts stabilized with the completion of lung alveolarization in rats. Our findings indicate a close association between platelet biogenesis and alveolarization in the developing lung. This phenomenon might explain the reduced platelet count in extremely premature infants with BPD.
支气管肺发育不良（BPD）是一种新生儿慢性肺部疾病，其特征为肺泡和血管发育停滞。BPD继发于肺不成熟、机械通气所致的肺损伤以及极早产儿暴露于高氧环境，会导致终身肺功能损害。近期研究表明，肺在血小板生成过程中发挥重要作用。然而，在肺发育及BPD发病机制中血小板生成的动态变化仍有待阐明。我们研究了极早产儿在BPD发生过程中以及新生大鼠从出生到成年正常发育过程中血小板参数的动态变化。我们还在通过长时间暴露于高氧诱导的实验性BPD大鼠模型中，进一步研究了高氧暴露对血小板生成及伴随的肺发育异常的影响。我们检测到极早产儿从出生到月经龄36周血小板计数呈生理性增加，但发生BPD的极早产儿血小板计数持续低于胎龄匹配的对照组。与临床研究结果一致，暴露于高氧显著降低了新生大鼠的血小板计数。肺形态计量学分析表明，大鼠肺泡化完成时血小板计数趋于稳定。我们的研究结果表明，在发育中的肺中血小板生成与肺泡化之间存在密切关联。这一现象可能解释了患有BPD的极早产儿血小板计数降低的原因。
