miR-200 family expression during normal and abnormal lung development due to congenital diaphragmatic hernia at the late
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ORIGINAL ARTICLE
miR‑200 family expression during normal and abnormal lung development due to congenital diaphragmatic hernia at the later embryonic stage in the nitrofen rat model Drew Mulhall1,2,3 · Naghmeh Khoshgoo1,2,3 · Robin Visser1,2,3 · Barbara Iwasiow1,2,3 · Chelsea Day1,2,3 · Fuqin Zhu1,2,3 · Patrice Eastwood4 · Richard Keijzer1,2,3,5 Accepted: 30 September 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Introduction Congenital diaphragmatic hernia (CDH) is a life-threatening disease associated with pulmonary hypoplasia. CDH occurs approximately 1 in every 2000–3000 live births, and the pathophysiology is unknown. MicroRNAs are short, non-coding RNAs that control gene expression through post-transcriptional regulation. Based on our previous work, we hypothesized that the miR-200 family is differentially expressed in normal and abnormal lung development. We aimed to examine the expression of the miR-200 family during normal and hypoplastic lung development due to CDH. Methods We performed reverse transcriptase polymerase chain reaction (RT-qPCR) and fluorescent in situ hybridization (FISH) to study the expression levels and distribution of the miR-200 family members on embryonic day 21 (E21) rat control and nitrofen-induced hypoplastic CDH lungs. Results RT-qPCR showed up-regulation of miR-200a in hypoplastic CDH lungs. FISH showed contrasting expression patterns for miR- 200a, miR-200c, and miR-429 between control and hypoplastic CDH lungs, while we could not detect miR-141 in control and hypoplastic CDH lungs. Conclusion We demonstrate a specific expression pattern of miR-200 family members in hypoplastic CDH lungs different from control lungs. This study suggests that disruption of miR-200 family expression plays a role in the pathogenesis of pulmonary hypoplasia associated with CDH. Keywords Lung development · Genetics · Developmental biology · Epigenetics · microRNA · CDH
Introduction * Richard Keijzer [email protected] 1
Biology of Breathing Group, The Children’s Hospital Research Institute of Manitoba, University of Manitoba, Winnipeg, MB, Canada
2
Division of Pediatric Surgery, Pediatrics and Child Health, Department of Surgery, University of Manitoba, Winnipeg, MB, Canada
3
Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, MB, Canada
4
Department of Development and Regeneration, Cluster Organ Systems, Faculty of Medicine, Katholieke Universiteit Leuven, Leuven, Belgium
5
Thorlakson Chair in Surgical Research, AE402 Harry Medovy House, 671 William Avenue, Winnipeg, MB R3E 0Z2, Canada
Congenital diaphragmatic hernia (CDH) is a life-threatening developmental defect of the diaphragm that causes migration of abdominal organs into the thoracic cavity [1]. CDH occurs with an incidence of approximately 1 in 2000 live births and is associated with pulmonary hypoplasia and persistent pulmonary hypertension [2, 3]. The genetic cause of ~ 85% of patients with CDH is unknown, which suggests that epigenetics may contr
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