PMID- 29136944
OWN - NLM
STAT- MEDLINE
DCOM- 20180803
LR  - 20220408
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 97
DP  - 2018 Jan
TI  - MIAT promotes proliferation and hinders apoptosis by modulating miR-181b/STAT3 
      axis in ox-LDL-induced atherosclerosis cell models.
PG  - 1078-1085
LID - S0753-3322(17)34059-3 [pii]
LID - 10.1016/j.biopha.2017.11.052 [doi]
AB  - BACKGROUND: Plenty of lncRNAs and microRNAs have been identified to be critical 
      mediators in the progression of atherosclerosis (AS). Myocardial 
      infarction-associated transcript (MIAT) were aberrantly high expressed and 
      closely associated with the pathogenesis of AS. However, its molecular mechanism 
      has not been well characterized. METHODS: The expression patterns of MIAT and 
      microRNA-181b (miR-181b) in clinical samples and cells were measured by RT-qPCR 
      assays. Luciferase reporter assay and RIP assays were used to manifest the 
      potential interaction between MIAT, miR-181b and signal transducer and activator 
      of transcription 3 (STAT3). Cell Counting Kit-8 (CCK-8), Propidium Iodide (PI) 
      staining, Terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end 
      labeling (TUNEL) and western blot assays were carried out to detect cell 
      proliferation, cell cycle distribution, apoptosis, and STAT3 protein level, 
      respectively. RESULTS: MIAT expression was up-regulated and miR-181b expression 
      was down-regulated in AS patients serum and oxidized low-density lipoprotein 
      (ox-LDL) induced AS cells model. MIAT facilitated cell proliferation, accelerated 
      cell cycle progression and inhibited apoptosis in ox-LDL-induced AS cell lines, 
      while this effect was partly reversed by miR-181b overexpression. Moreover, MIAT 
      enhanced STAT3 expression through sequestering miR-181b as a molecular sponge. 
      Furthermore, MiR-181b hindered cell growth, induced cell cycle arrest and 
      promoted apoptosis by directly targeting STAT3. CONCLUSION: MIAT performed as an 
      induction factor of AS by regulating miR-181b/STAT3 axis in ox-LDL-induced AS 
      cell lines, offering a new insight into the potential application of MIAT in AS 
      treatment.
CI  - Copyright (c) 2017 Elsevier Masson SAS. All rights reserved.
FAU - Zhong, Xiaoming
AU  - Zhong X
AD  - Department of Cardiology, Huaihe Hospital of Henan University, No. 8, Baobei 
      Road, Gulou District, Kaifeng, 475000, China.
FAU - Ma, Xiang
AU  - Ma X
AD  - Department of Cardiology, Huaihe Hospital of Henan University, No. 8, Baobei 
      Road, Gulou District, Kaifeng, 475000, China.
FAU - Zhang, Lei
AU  - Zhang L
AD  - Department of Cardiology, Huaihe Hospital of Henan University, No. 8, Baobei 
      Road, Gulou District, Kaifeng, 475000, China.
FAU - Li, Yanming
AU  - Li Y
AD  - Department of Cardiology, Huaihe Hospital of Henan University, No. 8, Baobei 
      Road, Gulou District, Kaifeng, 475000, China. Electronic address: 
      yanminglilym@163.com.
FAU - Li, Yunwei
AU  - Li Y
AD  - Department of Cardiology, Huaihe Hospital of Henan University, No. 8, Baobei 
      Road, Gulou District, Kaifeng, 475000, China.
FAU - He, Ruili
AU  - He R
AD  - Department of Cardiology, Huaihe Hospital of Henan University, No. 8, Baobei 
      Road, Gulou District, Kaifeng, 475000, China.
LA  - eng
PT  - Journal Article
DEP - 20171110
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (MIrn181 microRNA, human)
RN  - 0 (Miat long non-coding RNA)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (oxidized low density lipoprotein)
SB  - IM
MH  - Aged
MH  - Apoptosis/genetics
MH  - Atherosclerosis/genetics/*pathology
MH  - Blotting, Western
MH  - Case-Control Studies
MH  - Cell Cycle/genetics
MH  - Cell Cycle Checkpoints/genetics
MH  - Cell Proliferation/genetics
MH  - Cells, Cultured
MH  - Down-Regulation/genetics
MH  - Female
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Lipoproteins, LDL/administration & dosage
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Middle Aged
MH  - RNA, Long Noncoding/*genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - STAT3 Transcription Factor/*genetics
MH  - Up-Regulation/genetics
OTO - NOTNLM
OT  - Atherosclerosis
OT  - MIAT
OT  - STAT3
OT  - miR-181b
EDAT- 2017/11/16 06:00
MHDA- 2018/08/04 06:00
CRDT- 2017/11/16 06:00
PHST- 2017/08/10 00:00 [received]
PHST- 2017/10/17 00:00 [revised]
PHST- 2017/11/07 00:00 [accepted]
PHST- 2017/11/16 06:00 [pubmed]
PHST- 2018/08/04 06:00 [medline]
PHST- 2017/11/16 06:00 [entrez]
AID - S0753-3322(17)34059-3 [pii]
AID - 10.1016/j.biopha.2017.11.052 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2018 Jan;97:1078-1085. doi: 10.1016/j.biopha.2017.11.052. 
      Epub 2017 Nov 10.