PMID- 31702805
OWN - NLM
STAT- MEDLINE
DCOM- 20200406
LR  - 20200408
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 20
IP  - 6
DP  - 2019 Dec
TI  - miR‑21‑5p ameliorates hyperoxic acute lung injury and decreases apoptosis of 
      AEC II cells via PTEN/AKT signaling in rats.
PG  - 4953-4962
LID - 10.3892/mmr.2019.10779 [doi]
AB  - Inhibiting apoptosis of type II alveolar epithelial cells (AEC II) is an 
      effective way to decrease hyperoxic acute lung injury (HALI); however, the 
      specific underlying molecular mechanisms have not yet been fully elucidated. 
      Although miRNA‑21‑5p has previously been reported to decrease H2O2‑induced AEC II 
      apoptosis by targeting PTEN in vitro, whether miR‑21‑5p can decrease HALI in vivo 
      and the downstream molecular mechanisms remain unclear. In the present study, 
      rats were endotracheally administered with an miR‑21‑5p‑encoding 
      (AAV‑6‑miR‑21‑5p) or a negative control adenovirus vector, and then a HALI model 
      was established by exposure to hyperoxia. At 3 weeks following the administration 
      of AAV‑6‑miR‑21‑5p, the severity of HALI was decreased, as evidenced by the 
      improved outcome of the oxygenation index, respiratory index, wet/dry weight 
      ratio and pathological scores of the HALI lungs. To further investigate the 
      underlying mechanisms, AEC II cells were isolated from the lungs of the 
      experimental rats and cultured. The expression levels of miR‑21‑5p and its target 
      gene, PTEN, were detected, as well as the levels of phosphorylated and total AKT. 
      In addition, the apoptosis rate of AEC II was detected by flow cytometry. The 
      results demonstrated that AAV‑6‑miR‑21‑5p administration increased the miR‑21‑5p 
      levels in primary AEC II cells, while it decreased the expression levels of PTEN. 
      miR‑21‑5p overexpression also increased AKT phosphorylation in AEC II cells from 
      the HALI lungs compared with that of the HALI alone group and the control virus 
      group. The present study indicated that miR‑21‑5p ameliorated HALI in vivo, which 
      may have resulted from the inhibition of PTEN/AKT‑induced apoptosis of AEC II 
      cells. These findings suggest that miR‑21‑5p and PTEN/AKT signaling might serve 
      as potential targets for HALI treatment.
FAU - Qin, Song
AU  - Qin S
AD  - Intensive Care Unit, Affiliated Hospital of Zunyi Medical University, Zunyi, 
      Guizhou 563000, P.R. China.
FAU - Wang, Hongliang
AU  - Wang H
AD  - Intensive Care Unit, Affiliated Hospital of Zunyi Medical University, Zunyi, 
      Guizhou 563000, P.R. China.
FAU - Liu, Guoyue
AU  - Liu G
AD  - Intensive Care Unit, Affiliated Hospital of Zunyi Medical University, Zunyi, 
      Guizhou 563000, P.R. China.
FAU - Mei, Hong
AU  - Mei H
AD  - Intensive Care Unit, Affiliated Hospital of Zunyi Medical University, Zunyi, 
      Guizhou 563000, P.R. China.
FAU - Chen, Miao
AU  - Chen M
AD  - Intensive Care Unit, Affiliated Hospital of Zunyi Medical University, Zunyi, 
      Guizhou 563000, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20191030
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Messenger)
RN  - 0 (mirn21 microRNA, rat)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (Pten protein, rat)
SB  - IM
MH  - Acute Lung Injury/*metabolism/pathology
MH  - Alveolar Epithelial Cells/*metabolism
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Disease Models, Animal
MH  - Female
MH  - Hyperoxia/*metabolism
MH  - Lung/pathology
MH  - Male
MH  - MicroRNAs/*metabolism
MH  - PTEN Phosphohydrolase/genetics/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
PMC - PMC6854583
EDAT- 2019/11/09 06:00
MHDA- 2020/04/09 06:00
PMCR- 2019/10/30
CRDT- 2019/11/09 06:00
PHST- 2019/07/04 00:00 [received]
PHST- 2019/10/04 00:00 [accepted]
PHST- 2019/11/09 06:00 [pubmed]
PHST- 2020/04/09 06:00 [medline]
PHST- 2019/11/09 06:00 [entrez]
PHST- 2019/10/30 00:00 [pmc-release]
AID - mmr-20-06-4953 [pii]
AID - 10.3892/mmr.2019.10779 [doi]
PST - ppublish
SO  - Mol Med Rep. 2019 Dec;20(6):4953-4962. doi: 10.3892/mmr.2019.10779. Epub 2019 Oct 
      30.