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
link.springer.com shows its articles on its own site.
Read the article on link.springer.com ↗Article · Oct 2020 · 1 min read
In brief
In brief
Study examines miR-200 family microRNA expression in nitrofen-induced CDH rat model, finding upregulated miR-200a and altered expression patterns in hypoplastic lungs compared to controls. Results suggest disrupted miR-200 family regulation contributes to pulmonary hypoplasia pathogenesis in CDH, offering potential molecular targets for understanding this life-threatening congenital condition.
Written by the GCMD Library team from the article.
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.