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Identification of microRNAs changed in the neonatal lungs in response to hyperoxia exposure
Manoj Bhaskaran1, Dong Xi, Yang Wang
1The Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Department of Physiological Sciences, Oklahoma State University, Stillwater, Oklahoma, OK 74078, USA.
Abstract:
Bronchopulmonary dysplasia (BPD) is a multifactorial chronic lung disease of premature infants. BPD can be attributed to the dysregulation of normal lung development due to ventilation and oxygen toxicity, resulting in pathologic complications of impaired alveolarization and vascularization. MicroRNAs (miRNA) are small noncoding RNAs that regulate gene expression posttranscriptionally and are implicated in diverse biological processes and diseases. The objectives of this study are to identify the changed miRNAs and their target genes in neonatal rat lungs in response to hyperoxia exposure. Using miRNA microarray and real-time PCR analyses, we found downregulation of five miRNAs, miR-342, miR-335, miR-150, miR-126*, and miR-151*, and upregulation of two miRNAs, miR-21 and miR-34a. Some of these miRNAs had the highest expression during embryonic and early postnatal development. DNA microarray analysis yielded several genes with conserved binding sites for these altered miRNAs. Glycoprotein nonmetastatic melanoma protein b (GPNMB) was experimentally verified as a target of miR-150. In summary, we identified seven miRNAs that were changed in hyperoxia-exposed neonatal lungs. These results provide a basis for deciphering the mechanisms involved in the spatial and temporal regulation of proteins that contribute to the pathogenesis of BPD.
Insights
This study identified seven microRNAs (miRNAs) altered in neonatal rat lungs exposed to hyperoxia, a key factor in bronchopulmonary dysplasia (BPD) development. These findings offer insights into the molecular mechanisms underlying BPD pathogenesis.
Area of Science:
- Neonatal lung development
- Molecular biology
- Gene regulation
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants, often caused by ventilation and oxygen toxicity.
- This leads to impaired lung alveolarization and vascularization, disrupting normal lung development.
- MicroRNAs (miRNAs) are crucial regulators of gene expression involved in various biological processes and diseases.
Purpose of the Study:
- To identify specific miRNAs and their target genes that are altered in neonatal rat lungs due to hyperoxia exposure.
- To understand the role of these miRNAs in the pathogenesis of bronchopulmonary dysplasia.
Main Methods:
- Utilized miRNA microarray and real-time PCR to analyze miRNA expression changes in neonatal rat lungs.
- Employed DNA microarray analysis to identify potential target genes with conserved miRNA binding sites.
- Experimentally validated Glycoprotein nonmetastatic melanoma protein b (GPNMB) as a target of miR-150.
Main Results:
- Identified downregulation of five miRNAs (miR-342, miR-335, miR-150, miR-126*, miR-151*) and upregulation of two miRNAs (miR-21, miR-34a) in response to hyperoxia.
- Observed that some of these dysregulated miRNAs exhibit peak expression during critical embryonic and early postnatal development stages.
- Confirmed GPNMB as a direct target gene regulated by miR-150.
Conclusions:
- Seven specific miRNAs were found to be significantly changed in neonatal rat lungs under hyperoxia conditions.
- These findings provide a foundation for further research into the molecular mechanisms governing protein regulation in BPD.
- Understanding miRNA-mediated gene regulation is critical for developing therapeutic strategies for BPD.
