PMID- 32655407
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 11
DP  - 2020
TI  - Long Noncoding RNA TCONS_00016406 Attenuates Lipopolysaccharide-Induced Acute 
      Kidney Injury by Regulating the miR-687/PTEN Pathway.
PG  - 622
LID - 10.3389/fphys.2020.00622 [doi]
LID - 622
AB  - Acute kidney injury (AKI) is a common and serious complication of sepsis 
      accompanied by kidney dysfunction resulting from various etiologies and 
      pathophysiological processes. Unfortunately, there is currently no ideal 
      therapeutic strategy for AKI. Numerous studies have confirmed that long noncoding 
      RNAs (lncRNAs) play important regulatory roles in the pathogenesis of 
      sepsis-associated AKI. In this study, lncRNA TCONS_00016406 (termed lncRNA 6406), 
      a novel lncRNA identified by using TargetScan, was significantly downregulated in 
      the kidney tissues of mice with sepsis-associated AKI. This study aimed to 
      explore the role of lncRNA 6406 in lipopolysaccharide (LPS)-induced AKI and its 
      potential molecular mechanism. The models of sepsis-induced AKI (called 
      LPS-induced AKI models) in mice and cell lines were established with male C57BL/6 
      mice and renal tubular epithelial (PTEC) cells, respectively. Twenty-four hours 
      after LPS administration, kidneys and cell samples were collected after various 
      treatments to examine the alterations in the lncRNA 6406 levels and to evaluate 
      the effects on LPS-induced inflammation, oxidative stress, and apoptosis through 
      real-time PCR (RT-PCR) analysis, western blotting, and terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) staining. The results 
      revealed that lncRNA 6406 could significantly attenuate LPS-induced AKI, as shown 
      by the alleviation of inflammation, the suppression of oxidative stress and the 
      inhibition of apoptosis. Mechanistically, a luciferase reporter assay and 
      additional research showed that lncRNA 6406 functioned as a ceRNA to sponge 
      miRNA-687, thereby modulating LPS-stimulated AKI by targeting the miR-687/PTEN 
      axis; thus, this study presents a novel therapeutic strategy or sepsis-associated 
      AKI.
CI  - Copyright (c) 2020 Liu, Zhu, Zhang and Xu.
FAU - Liu, Xuelan
AU  - Liu X
AD  - Department of Emergency, Ningbo Medical Center Li Huili Hospital, Ningbo, China.
FAU - Zhu, Na
AU  - Zhu N
AD  - Department of Emergency, Ningbo Medical Center Li Huili Hospital, Ningbo, China.
FAU - Zhang, Bo
AU  - Zhang B
AD  - Department of Emergency, Ningbo Medical Center Li Huili Hospital, Ningbo, China.
FAU - Xu, Shao Bo
AU  - Xu SB
AD  - Department of Emergency, Ningbo Medical Center Li Huili Hospital, Ningbo, China.
LA  - eng
PT  - Journal Article
DEP - 20200618
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC7325890
OTO - NOTNLM
OT  - PTEN
OT  - acute kidney injury
OT  - long noncoding RNA 6406
OT  - miR-687
OT  - sepsis
EDAT- 2020/07/14 06:00
MHDA- 2020/07/14 06:01
PMCR- 2020/06/18
CRDT- 2020/07/14 06:00
PHST- 2020/02/07 00:00 [received]
PHST- 2020/05/18 00:00 [accepted]
PHST- 2020/07/14 06:00 [entrez]
PHST- 2020/07/14 06:00 [pubmed]
PHST- 2020/07/14 06:01 [medline]
PHST- 2020/06/18 00:00 [pmc-release]
AID - 10.3389/fphys.2020.00622 [doi]
PST - epublish
SO  - Front Physiol. 2020 Jun 18;11:622. doi: 10.3389/fphys.2020.00622. eCollection 
      2020.