LINC00052 ameliorates acute kidney injury by sponging miR-532-3p and activating the Wnt signaling pathway.
Acute Kidney Injury
/ etiology
Animals
Apoptosis
/ genetics
Cell Hypoxia
/ genetics
Cell Proliferation
/ genetics
Cyclin D1
/ metabolism
Humans
Kidney
/ metabolism
Malondialdehyde
/ metabolism
MicroRNAs
/ genetics
Proto-Oncogene Proteins c-myc
/ metabolism
RNA, Long Noncoding
/ genetics
Rats
Reactive Oxygen Species
/ metabolism
Reperfusion Injury
/ complications
Superoxide Dismutase
/ metabolism
Up-Regulation
Wnt Signaling Pathway
/ genetics
LINC00052
Wnt signaling
acute kidney injury
miR-532-3p
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
24 11 2020
24 11 2020
Historique:
received:
05
01
2020
accepted:
30
07
2020
pubmed:
25
11
2020
medline:
13
5
2021
entrez:
24
11
2020
Statut:
ppublish
Résumé
Acute kidney injury (AKI) is a complex renal disease. Long non-coding RNAs (lncRNAs) have frequently been associated with AKI. In the present study, we aimed to investigate the molecular mechanism(s) of LINC00052 in AKI. We found that LINC00052 expression was significantly decreased in AKI patient serum. In addition, in a hypoxic AKI cell model, LINC00052 expression was strongly elevated. In an I/R-triggered AKI rat model, the expression of TNF-α, IL-6 and IL-1β mRNA was strongly elevated. Moreover, we predicted miR-532-3p to be targeted by LINC00052 in AKI. Overexpression of LINC00052 increased hypoxia-induced inhibition of NRK-52E cell proliferation and reversed hypoxia-triggered apoptosis. Furthermore, we found that induction of TNF-α, IL-6 and IL-1β was repressed by overexpression of LINC00052. LINC00052 decreased hypoxia-induced ROS and MDA accumulation
Identifiants
pubmed: 33231561
pii: 104152
doi: 10.18632/aging.104152
pmc: PMC7835036
doi:
Substances chimiques
MIRN532 microRNA, human
0
MicroRNAs
0
Proto-Oncogene Proteins c-myc
0
RNA, Long Noncoding
0
Reactive Oxygen Species
0
Cyclin D1
136601-57-5
Malondialdehyde
4Y8F71G49Q
Superoxide Dismutase
EC 1.15.1.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
340-350Références
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