PMID- 33717243
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210316
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 21
IP  - 4
DP  - 2021 Apr
TI  - Attenuated macrophage activation mediated by microRNA-183 knockdown through 
      targeting NR4A2.
PG  - 300
LID - 10.3892/etm.2021.9731 [doi]
LID - 300
AB  - Atherosclerosis is considered a chronic inflammatory disease, and macrophages 
      function as important mediators in the development of atherogenesis. MicroRNA 
      (miR)-183 is a small non-coding RNA that acts as a novel tumor suppressor and has 
      recently been proposed to affect cardiac hypertrophy. However, the exact role and 
      underlying mechanism of miR-183 in macrophage activation remain unknown. In the 
      present study, miR-183 showed upregulated expression in atheromatous plaques and 
      in bone marrow-derived macrophages (BMDMs) subjected to stimulation with oxidized 
      low-density lipoproteins. Using a miR-183 loss-of-function strategy, it was 
      demonstrated that miR-183 knockdown significantly increased resolving M2 
      macrophage marker expression but decreased proinflammatory M1 macrophage marker 
      expression, as well as attenuated NF-kappaB activation. Moreover, decreased foam-cell 
      formation accompanied by upregulation of genes involved in cholesterol efflux and 
      downregulation of genes implicated in cholesterol influx was found in BMDMs 
      transfected with a miR-183 inhibitor. Mechanistically, macrophage activation 
      mediated by miR-183 silencing was partially attributed to direct upregulation of 
      NR4A2 expression in BMDMs. Thus, the present study suggests that neutralizing 
      miR-183 may be a potential therapeutic strategy for the treatment of 
      atherosclerosis.
CI  - Copyright (c) 2020, Spandidos Publications.
FAU - Gong, Fu-Han
AU  - Gong FH
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
FAU - Long, Li
AU  - Long L
AD  - Department of Clinical Laboratory, Tongren Municipal People's Hospital, Tongren, 
      Guizhou 554300, P.R. China.
FAU - Yang, Yong-Sheng
AU  - Yang YS
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
FAU - Shen, De-Hong
AU  - Shen DH
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
FAU - Zhang, Yu-Song
AU  - Zhang YS
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
FAU - Wang, Xue-Sheng
AU  - Wang XS
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
FAU - Zhang, Xue-Ping
AU  - Zhang XP
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
FAU - Xiao, Xiao-Qiang
AU  - Xiao XQ
AD  - Department of Cardiology, Tongren Municipal People's Hospital, Tongren, Guizhou 
      554300, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20210129
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC7885059
OTO - NOTNLM
OT  - NR4A2
OT  - atherosclerosis
OT  - inflammation
OT  - macrophage
OT  - microRNA-183
EDAT- 2021/03/16 06:00
MHDA- 2021/03/16 06:01
PMCR- 2021/01/29
CRDT- 2021/03/15 06:59
PHST- 2020/07/06 00:00 [received]
PHST- 2020/12/30 00:00 [accepted]
PHST- 2021/03/15 06:59 [entrez]
PHST- 2021/03/16 06:00 [pubmed]
PHST- 2021/03/16 06:01 [medline]
PHST- 2021/01/29 00:00 [pmc-release]
AID - ETM-0-0-09731 [pii]
AID - 10.3892/etm.2021.9731 [doi]
PST - ppublish
SO  - Exp Ther Med. 2021 Apr;21(4):300. doi: 10.3892/etm.2021.9731. Epub 2021 Jan 29.