Salusin-β mediates tubular cell apoptosis in acute kidney injury: Involvement of the PKC/ROS signaling pathway.
Acute Kidney Injury
/ chemically induced
Animals
Apoptosis
Cell Line
Cisplatin
/ adverse effects
Disease Models, Animal
Humans
Intercellular Signaling Peptides and Proteins
/ genetics
Kidney Tubules
/ cytology
Lipopolysaccharides
/ adverse effects
Male
Mice
Phosphorylation
Protein Kinase C
/ metabolism
Reactive Oxygen Species
/ metabolism
Signal Transduction
Up-Regulation
Apoptosis
Cisplatin
DNA damage
LPS
Oxidative stress
Salusin
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
12
11
2019
revised:
18
12
2019
accepted:
18
12
2019
pubmed:
31
12
2019
medline:
17
4
2021
entrez:
30
12
2019
Statut:
ppublish
Résumé
Salusin-β is abundantly expressed in many organs and tissues including heart, blood vessels, brain and kidneys. Recent studies have identified salusin-β as a bioactive peptide that contributes to various diseases, such as atherosclerosis, hypertension, diabetes and metabolic syndrome. However, the role of salusin-β in the pathogenesis of acute kidney injury (AKI) is largely unclear. In the present study, we investigated the roles of salusin-β in cisplatin or lipopolysaccharide (LPS)-induced renal injury. Herein, we found that salusin-β expression was upregulated in both renal tubular cells and kidney tissues induced by both cisplatin and LPS. In vitro, silencing of salusin-β diminished, whereas overexpression of salusin-β exaggerated the increased PKC phosphorylation, oxidative stress, histone γH2AX expression, p53 activation and apoptosis in either cisplatin or LPS-challenged renal tubular cells. More importantly, salusin-β overexpression-induced tubular cell apoptosis were abolished by using the PKC inhibitor Go 6976, reactive oxygen species (ROS) scavenger NAC, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin (Apo) or p53 inhibitor Pifithrin-α. In animals, blockade of salusin-β alleviated PKC phosphorylation, ROS accumulation, DNA damage, and p53 activation as well as renal dysfunction in mice after administration of cisplatin or LPS. Taken together, these results suggest that overexpressed salusin-β is deleterious in AKI by activation of the PKC/ROS signaling pathway, thereby priming renal tubular cells for apoptosis and death.
Identifiants
pubmed: 31884071
pii: S2213-2317(19)31385-0
doi: 10.1016/j.redox.2019.101411
pmc: PMC6939056
pii:
doi:
Substances chimiques
Intercellular Signaling Peptides and Proteins
0
Lipopolysaccharides
0
Reactive Oxygen Species
0
TOR2A protein, human
0
Protein Kinase C
EC 2.7.11.13
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101411Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest None.
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