The RNA-binding protein quaking is upregulated in nitrofen-induced congenital diaphragmatic hernia lungs at the end of gestation
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In brief
In brief
This study demonstrates that the RNA-binding protein Quaking (QKI) is significantly upregulated in late-gestation lungs of rats with nitrofen-induced congenital diaphragmatic hernia compared to controls. The findings suggest QKI dysregulation may contribute to abnormal lung development in CDH, offering potential insights into disease pathogenesis.
- QKI protein isoforms (QKI5, QKI6, QKI7) are significantly upregulated in CDH lungs at E21 compared to controls.
- IL-6 protein abundance is elevated in nitrofen-induced CDH lungs at end of gestation, suggesting inflammatory involvement.
- QKI dysregulation in late pregnancy may contribute to abnormal lung development pathogenesis in CDH.
- All three QKI isoforms show 1.48-1.63 fold increased mRNA expression in E21 CDH lungs (p<0.02 for all).
- QKI's role in epithelial-mesenchymal transition may be relevant to CDH lung hypoplasia mechanisms.
Written by the GCMD Library team from the article.
Abstract
Background
The RNA-binding protein Quaking (QKI) increases during epithelial-to-mesenchymal transition and its expression is controlled by microRNA-200 family members. Here, we aimed to describe the expression of QKI in the developing lungs of control and nitrofen-induced congenital diaphragmatic hernia lungs (CDH).
Methods
To investigate the expression of QKI, we dissected lungs from control and nitrofen-induced CDH rats on embryonic day 15, 18, 21 (E15, E18, E21). We performed immunofluorescence (IF) and quantitative reverse transcription PCR (RT-qPCR) for QKI expression. Additionally, we assessed Interleukin-6 (IL-6) abundance using IF.
Results
On E21, IF showed that the abundance of all three QKI isoforms and IL-6 protein was higher in CDH lungs compared to control lungs (QKI5: p = 0.023, QKI6: p = 0.006, QKI7: p = 0.014, IL-6: p = 0.045, respectively). Furthermore, RT-qPCR data showed increased expression of QKI5, QKI6, and QKI7 mRNA in E21 nitrofen lungs by 1.63 fold (p = 0.001), 1.63 fold (p = 0.010), and 1.48 fold (p = 0.018), respectively.
Conclusions
Our data show an increase in the abundance and expression of QKI at the end of gestation in nitrofen-induced CDH lungs. Therefore, a disruption in the regulation of QKI during the late stage of pregnancy could be associated with the pathogenesis of abnormal lung development in CDH.