PMID- 34539825
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210921
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Print)
IS  - 1792-0981 (Linking)
VI  - 22
IP  - 5
DP  - 2021 Nov
TI  - Long non-coding RNA TUG1 accelerates abnormal growth of airway smooth muscle 
      cells in asthma by targeting the miR-138-5p/E2F3 axis.
PG  - 1229
LID - 10.3892/etm.2021.10663 [doi]
LID - 1229
AB  - Asthma is a chronic airway inflammatory disease. The present study aimed to 
      explore the effect of the long non-coding RNA taurine-upregulated gene 1 (TUG1) 
      on the viability and migration of airway smooth muscle cells (ASMCs) in asthma. 
      Rat asthma models were constructed with ovalbumin sensitization and challenge and 
      the level of serum immunoglobulin E (IgE) and the rates of inspiratory and 
      expiratory resistance were measured. Reverse transcription-quantitative PCR was 
      also performed to determine the expression levels of TUG1. Platelet-derived 
      growth factor-BB (PDGF-BB)-treated ASMCs were then used as a cell model of 
      asthma. The viability and migratory abilities of ASMCs were analysed with the MTT 
      and Transwell assays. Additionally, a dual-luciferase reporter assay was used to 
      confirm the relationship between TUG1 and microRNA (miR)-138-5p and between 
      transcription factor E2F3 and miR-138-5p. The expression of TUG1, level of serum 
      IgE, inspiratory resistance and expiratory resistance were clearly increased in 
      the rat asthma model in comparison with controls. Knockdown of TUG1 the viability 
      and migration of PDGF-BB-induced ASMCs and reduced the inspiratory and expiratory 
      resistances. In addition, TUG1 functioned as a bait of miR-138-5p, and miR-138-5p 
      modulated E2F3 expression. Knockdown of E2F3 hindered the abnormal growth of 
      ASMCs. Moreover, miR-138-5p inhibition or E2F3 overexpression reversed the 
      inhibitory effects of TUG1 knockdown on viability and migration of 
      PDGF-BB-induced ASMCs. The TUG1/miR-138-5p/E2F3 regulatory axis appeared to play 
      a critical role in accelerating the viability and migration of ASMCs and may 
      therefore have a role in asthma.
CI  - Copyright (c) 2020, Spandidos Publications.
FAU - Zhou, Haiyin
AU  - Zhou H
AD  - Intensive Care Unit, Hunan Children's Hospital, Changsha, Hunan 410007, P.R. 
      China.
FAU - Long, Caixia
AU  - Long C
AD  - Intensive Care Unit, Hunan Children's Hospital, Changsha, Hunan 410007, P.R. 
      China.
FAU - Liu, Pingping
AU  - Liu P
AD  - Intensive Care Unit, Hunan Children's Hospital, Changsha, Hunan 410007, P.R. 
      China.
FAU - Chen, Yanying
AU  - Chen Y
AD  - Intensive Care Unit, Hunan Children's Hospital, Changsha, Hunan 410007, P.R. 
      China.
FAU - Luo, Lan
AU  - Luo L
AD  - Intensive Care Unit, Hunan Children's Hospital, Changsha, Hunan 410007, P.R. 
      China.
FAU - Xiao, Zhenghui
AU  - Xiao Z
AD  - Intensive Care Unit, Hunan Children's Hospital, Changsha, Hunan 410007, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20210827
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC8438697
OTO - NOTNLM
OT  - E2F3
OT  - airway smooth muscle cells
OT  - asthma
OT  - long non-coding RNA TUG1
OT  - microRNA-138-5p
COIS- The authors declare that they have no competing interests.
EDAT- 2021/09/21 06:00
MHDA- 2021/09/21 06:01
PMCR- 2021/08/27
CRDT- 2021/09/20 06:04
PHST- 2020/05/27 00:00 [received]
PHST- 2021/06/28 00:00 [accepted]
PHST- 2021/09/20 06:04 [entrez]
PHST- 2021/09/21 06:00 [pubmed]
PHST- 2021/09/21 06:01 [medline]
PHST- 2021/08/27 00:00 [pmc-release]
AID - ETM-0-0-10663 [pii]
AID - 10.3892/etm.2021.10663 [doi]
PST - ppublish
SO  - Exp Ther Med. 2021 Nov;22(5):1229. doi: 10.3892/etm.2021.10663. Epub 2021 Aug 27.