NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE108755 Query DataSets for GSE108755
Status Public on Jan 05, 2018
Title Differentially expressed genes in blood of BPD and Normal preterm neonates [miRNA]
Platform organism synthetic construct
Sample organism Homo sapiens
Experiment type Non-coding RNA profiling by array
Summary Bronchopulmonary dysplasia (BPD) is the major cause of chronic lung disease (CLD) and morbidity in preterm infants, which characterized by impaired pulmonary alveolar development in preterm infants. There is increasing evidence that micro RNA (miRNA) has a close association with the development of pulmonary diseasesincluding lung growth, pulmonary fibrosis, pneumonia, etc. The potential role of miRNA in the pathogenesis of BPD is unclear. This study aims to clarify the role of adrenomedullin (ADM) regulated by miRNA-547-3p during the process of BPD and illustrate the protective effect of ADM involved in preterm infants.We indentified the differential expressed miRNA and their potential target genes, microarray analysis using Agilent Human 4x44K Gene Expression Microarrays v2 and miRCURY LNA™ microRNA Array was performed. The results of miRNA chip were scanned by Axon GenePix 4000B and the signal of probes were read by GenePix Pro 6.0 software. Only the target genes which exist in both two databases and having different expression trend were remained. Thus, miRNA-574-3p and it’s target gene ADM were selected to do the further research in our study. And we verified miRNA-574-3p and ADM expression in BPD premature infants by realtime q-PCR. After the microarray expression analysis, there were 516 probes differential expressed between BPD samples and normal samples. Among them, 510 were up-regulated and 213 were down-regulated. Meanwhile, to the miRNA aspect, there were 37 up-regulated and 44 down-regulated. After text mining, we found ADM was already found play a role in BPD. ADM is an endogenous peptide with potent angiogenic, anti-oxidant, and anti-inflammatory properties. Realtime q-PCR assay results showed that, miRNA-574-3p expression level in blood samples from preterm infants with BPD was significantly decreased, ADM expression level in blood samples from preterm infants with BPD was significantly increased. In our study, we found that up-regulation of ADM regulated by miRNA-574-3p could protect preterm infants with BPD. These data provide novel insights into ADM regulated by miRNA-574-3p which may be shed light on BPD prevention and treatment.
 
Overall design The differential expressed genes in in blood of BPD and Normal preterm neonates were measured. Five independent experiments were performed using different donors for each experiment.
 
Contributor(s) Gong X, Qiu J, Ma L, Qiu G, Shen Y, Yan C, Cai C
Citation missing Has this study been published? Please login to update or notify GEO.
Submission date Jan 04, 2018
Last update date Jan 24, 2018
Contact name cai cheng
E-mail(s) caicheng2004@163.com
Organization name Shanghai Children’s Hospital, Shanghai Jiao Tong University
Department Department of neonatology
Street address No. 355, Luding Road
City Shanghai
ZIP/Postal code 200062
Country China
 
Platforms (1)
GPL17107 Exiqon miRCURY LNA™ microRNA Array - hsa, mmu & rno
Samples (11)
GSM2912963 ExVivoBlood_BPD_rep1_miRNA
GSM2912964 ExVivoBlood_BPD_rep2_miRNA
GSM2912965 ExVivoBlood_BPD_rep3_miRNA
This SubSeries is part of SuperSeries:
GSE108756 Differentially expressed genes in blood of BPD and Normal preterm neonates
Relations
BioProject PRJNA428504

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE108755_RAW.tar 10.1 Mb (http)(custom) TAR (of GPR)
GSE108755_normalized_data_matrix.txt.gz 117.4 Kb (ftp)(http) TXT
Processed data are available on Series record

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap