Send to

Choose Destination
Cell Biochem Funct. 2016 Jul;34(5):299-309. doi: 10.1002/cbf.3190. Epub 2016 May 3.

Differential expression of long non-coding RNAs in hyperoxia-induced bronchopulmonary dysplasia.

Author information

Department of Neonatology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China.
Neonatal Medical Centre, Huai'an Maternity and Child Healthcare Hospital, Huai'an, Jiangsu, China.
Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.


Bronchopulmonary dysplasia (BPD) is a common complication of premature birth that seriously affects the survival rate and quality of life among preterm neonates. Long non-coding RNAs (lncRNAs) have been implicated in many human diseases. However, the role of lncRNAs in the pathogenesis of BPD remains poorly understood. Here, we exposed neonatal C57BL/6J mice to 95% concentrations of ambient oxygen and established a mouse lung injury model that mimicked human BPD. Next, we compared lncRNA and messenger RNA (mRNA) expression profiles between BPD and normal lung tissues using a high-throughput mouse lncRNA + mRNA array system. Compared with the control group, 882 lncRNAs were upregulated, and 887 lncRNAs were downregulated in BPD lung tissues. We validated some candidate BPD-associated lncRNAs by real-time quantitative reverse-transcription polymerase chain reaction analysis in eight pairs of BPD and normal lung tissues. Gene ontology, pathway and bioinformatics analyses revealed that a downregulated lncRNA, namely AK033210, associated with tenascin C may be involved in the pathogenesis of BPD. To the best of our knowledge, our study is the first to reveal differential lncRNA expression in BPD, which provides a foundation for further understanding of the molecular mechanism of BPD development.


bronchopulmonary dysplasia; hyperoxia; long non-coding RNA; microarray analysis

[Indexed for MEDLINE]

Supplemental Content

Loading ...
Support Center