DIFFERENTIALLY EXPRESSED CIRCULATING LONG-NONCODING RNAS IN PREMATURE INFANTS WITH RESPIRATORY DISTRESS SYNDROME
Bao ZD, Wan J, Zhu W, Shen JX, Yang Y, Zhou XY
*Corresponding Author: Dr. Yang Yang and Dr. Zhou Xiao‑Yu, E‑mail: yy860507@126.com (YY) and xyzhou161@163.com (XYZ), Tel:+ 86-25-83117362, Department of Neonatology, Children’s Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China
page: 11
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Abstract
Purpose: Recent studies have addressed the association
between lung development and long-noncoding RNAs
(lncRNAs). But few studies have investigated the role of
lncRNAs in neonatal respiratory distress syndrome (RDS).
Thus, this study aimed to compare the expression profile
of circulating lncRNAs between RDS infants and controls.
Methods: 10 RDS infants and 5 controls were enrolled.
RDS patients were further divided into mild and
severe RDS subgroups. Blood samples were collected for
the lncRNA expression profile. Subsequently, differentially
expressed lncRNAs were screened out. Bioinformatics
analysis was applied to establish a co-expression network
of differential lncRNAs and mRNAs, and predict the underlying
biological functions.
Results: A total of 135 differentially expressed lncRNAs
were identified, including 108 upregulated and
27 downregulated lncRNAs (fold-change>2 and P<0.05)
among the three groups (non-RDS, mild RDS and severe
RDS groups). Of these lncRNAs, four were selected
as showing higher fold changes and validated by
qRT-PCR. ENST00000470527.1, ENST00000504497.1,
ENST00000417781.5, and ENST00000440408.5 were
increased not only in the plasma of total RDS patients but
also in the severe RDS subgroup. Gene Ontology (GO)
and Kyoto encyclopedia of genes and genomes (KEGG)
analyses showed that differentially expressed lncRNAs
may play important roles in RDS through regulating PI3KAkt,
RAS, MAPK, and TGF-β signaling pathways.
Conclusion: The present results found that
ENST00000470527.1,
ENST00000504497.1, ENST00000417781.5,
and ENST00000440408.5 may be involved
in RDS. This could provide new insight into research of the
potential pathophysiological mechanisms of preterm RDS.
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