Expression of long non-coding RNA NANCI in lung tissues of neonatal mice with hyperoxia-induced lung injury and its regulatory effect on NKX2.1.
- Author:
Yuan ZHANG
1
;
Huai-Ping CHENG
;
Tian-Ping BAO
;
Xiu-Gui WANG
;
Zhao-Fang TIAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Female; Hyperoxia; complications; Lung; metabolism; Lung Injury; etiology; Male; Mice; Mice, Inbred C57BL; Nuclear Proteins; physiology; RNA, Long Noncoding; physiology; Signal Transduction; physiology; Thyroid Nuclear Factor 1; Transcription Factors; physiology
- From: Chinese Journal of Contemporary Pediatrics 2017;19(2):215-221
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expression of long non-coding RNA NANCI in lung tissues of neonatal mice with hyperoxia-induced lung injury and its regulatory effect on NKX2.1.
METHODSA total of 48 neonatal C57BL/6J mice were randomly divided into an air group and a hyperoxia group, with 24 mice in each group. Each group was further divided into 7-day, 14-day, and 21-day subgroups, with 8 mice in each subgroup. The mice in the air group were fed in the indoor environment (FiO=21%) and those in the hyperoxia group were fed in a high-oxygen box (oxygen concentration: >95%). The mice were sacrificed at each time point and lung tissue samples were collected. Hematoxylin and eosin staining was used to observe pathological changes in lung tissues. RT-qPCR and Western blot were used to measure the mRNA and protein expression of NANCI and NKX2.1.
RESULTSThe air group had the highest mRNA expression of NANCI and NKX2.1 at 7 days and the same level of mRNA expression at 14 and 21 days. Compared with the air group, the hyperoxia group had significant reductions in the degree of alveolarization and radial alveolar count (RAC) in lung tissues (P<0.05), and in the hyperoxia group, RAC gradually decreased over the time of hyperoxia exposure (P<0.05). The hyperoxia group had significantly lower mRNA and protein expression of NANCI and NKX2.1 than the air group at all time points (P<0.05). In both groups, the relative mRNA and protein expression of NANCI and NKX2.1 gradually decreased over the time of hyperoxia exposure (P<0.05). The expression of NKX2 was positively correlated with that of NANCI (r=0.585, P=0.003), and the expression of NKX2 and NANCI was positively correlated with RAC in the hyperoxia group (r=0.655 and 0.541 respectively, P<0.05).
CONCLUSIONSNANCI may be involved in the development of immature lung tissues. Lung injury is gradually aggravated over the time of hyperoxia exposure. The levels of NANCI and NKX2.1 are associated with the severity of lung injury, suggesting that the NANCI/NKX2.1 target gene signaling pathway might be involved in the development of hyperoxia-induced lung injury in neonatal mice.
