The Long Noncoding RNA ANRIL Promotes Cell Apoptosis in Lipopolysaccharide-Induced Acute Kidney Injury Mediated by the TLR4/Nuclear Factor-Kappa B Pathway.
ANRIL
Acute kidney injury
Endotoxin
Nuclear factor-kappa B
miR-199a
Journal
Kidney & blood pressure research
ISSN: 1423-0143
Titre abrégé: Kidney Blood Press Res
Pays: Switzerland
ID NLM: 9610505
Informations de publication
Date de publication:
2020
2020
Historique:
received:
03
09
2019
accepted:
01
12
2019
pubmed:
19
2
2020
medline:
5
11
2020
entrez:
19
2
2020
Statut:
ppublish
Résumé
The purpose of this study is to analyze the expression and biological function of lncRNA ANRIL, microRNA-199a, TLR4, and nuclear factor-kappa B (NF-κB) in acute renal injury (AKI) induced by lipopolysaccharide (LPS). The levels of ANRIL and microRNA-199a in mouse cells and kidneys were detected by quantitative-polymerase chain reaction. Western blot analysis was used for the NF-κB pathway protein. MTT assay was used for cell viability. Enzyme-linked immunosorbent assay was used for the secretion of inflammatory factors in mouse kidney tissue. Apoptosis was measured by flow cytometry and Western blotting. The potential binding region between ANRIL and miR-199a was verified by luciferase reporter assay. The upregulation of ANRIL can reduce the expression of microRNA-199a and increases the number of apoptotic cells. The expression levels of ANRIL in LPS-induced AKI mice and LPS-treated HK2 cells were upregulated compared with the control group. Overexpression of ANRIL increased apoptosis and promoted TLR4 (Toll-like receptor 4), NF-κB phosphorylation, and downstream transcription factor production. ANRIL/NF-κB pathway in LPS-induced apoptosis provided theoretical guidance for ANRIL in the treatment of AKI.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
The purpose of this study is to analyze the expression and biological function of lncRNA ANRIL, microRNA-199a, TLR4, and nuclear factor-kappa B (NF-κB) in acute renal injury (AKI) induced by lipopolysaccharide (LPS).
METHODS
METHODS
The levels of ANRIL and microRNA-199a in mouse cells and kidneys were detected by quantitative-polymerase chain reaction. Western blot analysis was used for the NF-κB pathway protein. MTT assay was used for cell viability. Enzyme-linked immunosorbent assay was used for the secretion of inflammatory factors in mouse kidney tissue. Apoptosis was measured by flow cytometry and Western blotting. The potential binding region between ANRIL and miR-199a was verified by luciferase reporter assay.
RESULTS
RESULTS
The upregulation of ANRIL can reduce the expression of microRNA-199a and increases the number of apoptotic cells. The expression levels of ANRIL in LPS-induced AKI mice and LPS-treated HK2 cells were upregulated compared with the control group. Overexpression of ANRIL increased apoptosis and promoted TLR4 (Toll-like receptor 4), NF-κB phosphorylation, and downstream transcription factor production.
CONCLUSION
CONCLUSIONS
ANRIL/NF-κB pathway in LPS-induced apoptosis provided theoretical guidance for ANRIL in the treatment of AKI.
Identifiants
pubmed: 32069473
pii: 000505154
doi: 10.1159/000505154
doi:
Substances chimiques
Lipopolysaccharides
0
NF-kappa B
0
RNA, Long Noncoding
0
TLR4 protein, human
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
209-221Informations de copyright
© 2020 The Author(s) Published by S. Karger AG, Basel.