PMID- 29157986
OWN - NLM
STAT- MEDLINE
DCOM- 20180727
LR  - 20230523
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Linking)
VI  - 818
DP  - 2018 Jan 5
TI  - LncRNA myocardial infarction-associated transcript (MIAT) contributed to cardiac 
      hypertrophy by regulating TLR4 via miR-93.
PG  - 508-517
LID - S0014-2999(17)30764-1 [pii]
LID - 10.1016/j.ejphar.2017.11.031 [doi]
AB  - It has been reported that lncRNA myocardial infarction-associated transcript 
      (MIAT) facilitated the pathological development in angiotensin II (AngII)-induced 
      cardiac hypertrophy. Nevertheless, the underlying mechanism of MIAT involved in 
      cardiac hypertrophy is largely unknown. In this study, AngII-treated 
      cardiomyocytes were applied as a cardiac hypertrophy model in vitro. The 
      expressions of MIAT and miR-93 were detected by qRT-PCR. The protein levels of 
      toll-like receptor 4 (TLR4), atrial natriuretic factor (ANF), beta-myosin heavy 
      chain (beta-MHC), phosphoinositide-3 kinase (PI3K), protein kinase B (Akt), 
      phosphorylated Akt (p-Akt), mammalian target of rapamycin (mTOR), and 
      phosphorylated mTOR (p-mTOR) were determined by western blot. Luciferase reporter 
      assay and RNA immunoprecipitation (RIP) were performed to explore the 
      relationship between MIAT, TLR4 and miR-93. Hypertrophic response was assessed by 
      measuring cell surface area and quantifying the expressions of ANF and beta-MHC. The 
      results demonstrated that MIAT was upregulated and miR-93 was downregulated in 
      AngII-treated cardiomyocytes. MIAT functioned as a molecular sponge of miR-93 in 
      cardiomyocytes. Additionally, TLR4 was identified as a target of miR-93 and MIAT 
      promoted TLR4 expression by sponging miR-93. MIAT knockdown decreased cell 
      surface area and the expression levels of ANF and beta-MHC in AngII-treated 
      cardiomyocytes by modulating miR-93. Moreover, enforced expression of TLR4 
      partially reversed the protective effect of miR-93 overexpression on 
      AngII-induced cardiac hypertrophy. Furthermore, MIAT knockdown or miR-93 
      overexpression inactivated the PI3K/Akt/mTOR pathway via TLR4 in AngII-induced 
      cardiac hypertrophy. Taken together, these data suggested that MIAT knockdown 
      inhibited AngII-induced cardiac hypertrophy by regulating miR-93/TLR4 axis, 
      highlighting a promising therapy target for cardiac hypertrophy.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Li, Yunwei
AU  - Li Y
AD  - Department of Cardiology, Huaihe Hospital of Henan University, Kaifeng 475000, 
      China. Electronic address: liyunweiywl@126.com.
FAU - Wang, Juan
AU  - Wang J
AD  - Department of Cardiology, Huaihe Hospital of Henan University, Kaifeng 475000, 
      China.
FAU - Sun, Lili
AU  - Sun L
AD  - Department of Cardiology, Huaihe Hospital of Henan University, Kaifeng 475000, 
      China.
FAU - Zhu, Shengnan
AU  - Zhu S
AD  - Department of Cardiology, Huaihe Hospital of Henan University, Kaifeng 475000, 
      China.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20171121
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Miat long non-coding RNA)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn93 microRNA, rat)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Toll-Like Receptor 4)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
RIN - Eur J Pharmacol. 2023 Jul 5;950:175760. PMID: 37198077
MH  - Animals
MH  - Base Sequence
MH  - Cardiomegaly/*genetics/*metabolism/pathology
MH  - Gene Knockdown Techniques
MH  - MicroRNAs/*genetics
MH  - Myocytes, Cardiac/metabolism/pathology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Long Noncoding/*genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Signal Transduction/genetics
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Toll-Like Receptor 4/*genetics/*metabolism
MH  - Up-Regulation/genetics
OTO - NOTNLM
OT  - AngII
OT  - Cardiac hypertrophy
OT  - LncRNA
OT  - MIAT
OT  - MiR-93
OT  - TLR4
EDAT- 2017/11/22 06:00
MHDA- 2018/07/28 06:00
CRDT- 2017/11/22 06:00
PHST- 2017/09/13 00:00 [received]
PHST- 2017/11/14 00:00 [revised]
PHST- 2017/11/16 00:00 [accepted]
PHST- 2017/11/22 06:00 [pubmed]
PHST- 2018/07/28 06:00 [medline]
PHST- 2017/11/22 06:00 [entrez]
AID - S0014-2999(17)30764-1 [pii]
AID - 10.1016/j.ejphar.2017.11.031 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2018 Jan 5;818:508-517. doi: 10.1016/j.ejphar.2017.11.031. Epub 
      2017 Nov 21.