PMID- 31566734
OWN - NLM
STAT- MEDLINE
DCOM- 20210202
LR  - 20210202
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 235
IP  - 4
DP  - 2020 Apr
TI  - Long noncoding RNA MIAT2 alleviates lipopolysaccharide-induced inflammatory 
      damage in WI-38 cells by sponging microRNA-15.
PG  - 3690-3697
LID - 10.1002/jcp.29263 [doi]
AB  - Neonatal pneumonia is a high neonatal mortality disease. We studied the function 
      and mechanism of long noncoding RNA myocardial infarction-associated transcript 2 
      (lncRNA MIAT2) on lipopolysaccharide (LPS)-induced inflammation in WI-38 cells. 
      Cell Counting Kit-8 and apoptosis assay were respectively used to detect the 
      functions of LPS, MIAT2, and microRNA-15 (miR-15) on viability and apoptosis. 
      MIAT2 and miR-15 expressions were changed by cell transfection. Moreover, reverse 
      transcription-quantitative polymerase chain reaction (RT-qPCR), western blot, and 
      enzyme-linked immunosorbent assay were used to detect the expressions of 
      interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1). The levels of 
      Bax, cleaved-caspase-3, and cell pathways-related proteins were tested by western 
      blot. Besides, the levels of miR-15 and MIAT2 were tested by RT-qPCR. We found 
      that LPS declined cell viability and heightened apoptosis and levels of Bax, 
      cleaved-caspase-3, IL-6, and MCP-1. MIAT2 was negatively regulated by LPS and it 
      alleviated LPS-induced damage. Furthermore, MIAT2 reversely regulated miR-15 and 
      miR-15 mimic could reverse the effects of MIAT2. Finally, MIAT2 restrained the 
      p38MAPK and NF-kappaB pathways by downregulating miR-15. In conclusion, MIAT2 
      alleviated LPS-induced inflammation damage in WI-38 cells by sponging miR-15 via 
      p38MAPK and NF-kappaB pathways.
CI  - (c) 2019 Wiley Periodicals, Inc.
FAU - Zhang, Hong
AU  - Zhang H
AD  - Department of Pediatrics, Liaocheng People's Hospital, Liaocheng, Shandong, 
      China.
FAU - Zhao, Jing
AU  - Zhao J
AD  - Department of Pediatrics, Liaocheng People's Hospital, Liaocheng, Shandong, 
      China.
FAU - Shao, Peng
AU  - Shao P
AUID- ORCID: 0000-0001-9248-4564
AD  - Department of Pediatrics, Liaocheng People's Hospital, Liaocheng, Shandong, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20190930
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (MIRN15 microRNA, human)
RN  - 0 (Miat long non-coding RNA)
RN  - 0 (MicroRNAs)
RN  - 0 (RELA protein, human)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Apoptosis
MH  - Caspase 3/genetics
MH  - Cell Line
MH  - Cell Survival/genetics
MH  - Chemokine CCL2
MH  - Gene Expression Regulation/genetics
MH  - Humans
MH  - Infant, Newborn
MH  - Infant, Newborn, Diseases/genetics/pathology
MH  - Inflammation/chemically induced/*genetics/pathology
MH  - Interleukin-6/genetics
MH  - Lipopolysaccharides/toxicity
MH  - MicroRNAs/*genetics
MH  - Pneumonia/*genetics/pathology
MH  - RNA, Long Noncoding/*genetics
MH  - Signal Transduction/genetics
MH  - Transcription Factor RelA/genetics
MH  - bcl-2-Associated X Protein/genetics
OTO - NOTNLM
OT  - MIAT2
OT  - miR-15
OT  - neonatal pneumonia
OT  - p38MAPK and NF-kappaB pathways
EDAT- 2019/10/01 06:00
MHDA- 2021/02/03 06:00
CRDT- 2019/10/01 06:00
PHST- 2019/05/16 00:00 [received]
PHST- 2019/09/03 00:00 [accepted]
PHST- 2019/10/01 06:00 [pubmed]
PHST- 2021/02/03 06:00 [medline]
PHST- 2019/10/01 06:00 [entrez]
AID - 10.1002/jcp.29263 [doi]
PST - ppublish
SO  - J Cell Physiol. 2020 Apr;235(4):3690-3697. doi: 10.1002/jcp.29263. Epub 2019 Sep 
      30.