PMID- 31498515
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230201
IS  - 1095-8355 (Electronic)
IS  - 1065-6995 (Linking)
VI  - 44
IP  - 1
DP  - 2020 Jan
TI  - Long non-coding RNA MALAT1 sponges miR-149 to promote inflammatory responses of 
      LPS-induced acute lung injury by targeting MyD88.
PG  - 317-326
LID - 10.1002/cbin.11235 [doi]
AB  - Acute lung injury (ALI) caused by sepsis occurs early and the condition is 
      severe, and is also an important reason for accelerating the death of patients. 
      Increasing evidence has identified long non-coding RNA (lncRNA) metastasis 
      associated in lung adenocarcinoma transcript 1 (MALAT1) as a regulator of ALI. 
      However, the potential mechanism underlying MALAT1 on ALI still needs further 
      identification. To explore the mechanisms of gene regulation expression mediated 
      by MALAT1 through miR-149/MyD88 in lung injury inflammation, we constructed a 
      lung injury inflammatory model using the lipopolysaccharides (LPS)-induced method 
      and quantificated the cytokines and signaling cascade molecules as well as 
      miR-149. The MALAT1, myeloid differentiation factor 88 (MyD88), tumor necrosis 
      factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 levels were significantly 
      increased, and the nuclear factor-kappaB (NF-kappaB) pathway was activated, but the 
      miR-149 level was decreased in the LPS-induced ALI model. miR-149 directly 
      targeted both lncRNA MALAT1 and the MyD88 gene. Knockdown of MALAT1 
      down-regulated the levels of MyD88, TNF-alpha, IL-1beta, and IL-6, and inhibited the 
      NF-kappaB pathway. However, MALAT1 knockdown up-regulated the expression of miR-149. 
      Overexpression of miR-149 down-regulated MyD88, TNF-alpha, IL-1beta, and IL-6 levels, 
      and inhibited the NF-kappaB pathway. MALAT1 acts as a pro-inflammatory factor in ALI 
      via the miR-149/MyD88/NF-kappaB axis and is therefore a potential novel therapeutic 
      target for ALI treatment.
CI  - (c) 2019 International Federation for Cell Biology.
FAU - Liang, Wei-Jun
AU  - Liang WJ
AD  - Department of Respiratory Medicine, Changsha Central Hospital, Changsha, P.R. 
      China.
FAU - Zeng, Xiao-Yuan
AU  - Zeng XY
AD  - Department of Respiratory Medicine, Changsha Central Hospital, Changsha, P.R. 
      China.
FAU - Jiang, Sha-Li
AU  - Jiang SL
AD  - Department of Pathology, Changsha Central Hospital, Changsha, P.R. China.
FAU - Tan, Hong-Yi
AU  - Tan HY
AD  - Department of Respiratory Medicine, Changsha Central Hospital, Changsha, P.R. 
      China.
FAU - Yan, Mu-Yun
AU  - Yan MY
AD  - Department of Respiratory Medicine, Changsha Central Hospital, Changsha, P.R. 
      China.
FAU - Yang, Hong-Zhong
AU  - Yang HZ
AUID- ORCID: 0000-0002-5040-851X
AD  - Department of Respiratory Medicine, Changsha Central Hospital, Changsha, P.R. 
      China.
LA  - eng
GR  - B2017205/Medicine and Health Planned Project of Hunan Province/
PT  - Journal Article
DEP - 20190909
PL  - England
TA  - Cell Biol Int
JT  - Cell biology international
JID - 9307129
SB  - IM
OTO - NOTNLM
OT  - MALAT1
OT  - MyD88
OT  - acute lung injury
OT  - inflammatory
OT  - miR-149
EDAT- 2019/09/10 06:00
MHDA- 2019/09/10 06:01
CRDT- 2019/09/10 06:00
PHST- 2019/05/30 00:00 [received]
PHST- 2019/08/31 00:00 [accepted]
PHST- 2019/09/10 06:00 [pubmed]
PHST- 2019/09/10 06:01 [medline]
PHST- 2019/09/10 06:00 [entrez]
AID - 10.1002/cbin.11235 [doi]
PST - ppublish
SO  - Cell Biol Int. 2020 Jan;44(1):317-326. doi: 10.1002/cbin.11235. Epub 2019 Sep 9.