Renal Ischemia/Reperfusion Early Induces Myostatin and PCSK9 Expression in Rat Kidneys and HK-2 Cells.
Acute Kidney Injury
/ genetics
Animals
Disease Models, Animal
Humans
Hydrogen Peroxide
/ pharmacology
Kidney
/ injuries
Myostatin
/ genetics
Oxidative Stress
/ genetics
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
/ genetics
Proprotein Convertase 9
/ genetics
RNA, Messenger
/ genetics
Rats
Reactive Oxygen Species
/ metabolism
Reperfusion Injury
/ genetics
aorta cross-clamping
mitochondrial dysfunction
oxidative stress
renal injury
tubular necrosis
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
13 Sep 2021
13 Sep 2021
Historique:
received:
15
08
2021
revised:
01
09
2021
accepted:
03
09
2021
entrez:
28
9
2021
pubmed:
29
9
2021
medline:
21
10
2021
Statut:
epublish
Résumé
During visceral interventions, the transient clampage of supraceliac aorta causes ischemia/reperfusion (I/R) in kidneys, sometime resulting in acute renal failure; preclinical studies identified redox imbalance as the main driver of I/R injury. However, in humans, the metabolic/inflammatory responses seem to prevail on oxidative stress. We investigated myostatin (Mstn) and proprotein convertase subtilisin/kexin type 9 (PCSK9), proatherogenic mediators, during renal I/R. Compared to sham-operated animals, the kidneys of rats who had experienced ischemia (30 min) had higher Mstn and PCSK9 expression after 4 h of reperfusion. After 24 h, they displayed tubular necrosis, increased nitrotyrosine positivity, and nuclear peroxisome proliferator-activated receptor gamma coactivator-1alpha relocation, markers of oxidative stress and mitochondria imbalance. Mstn immunopositivity was increased in tubuli, while PCSK9 immunosignal was depleted; systemically, PCSK9 was higher in plasma from I/R rats. In HK-2 cells, both ischemia and reperfusion enhanced reactive oxygen species production and mitochondrial dysfunction. H
Identifiants
pubmed: 34576046
pii: ijms22189884
doi: 10.3390/ijms22189884
pmc: PMC8465118
pii:
doi:
Substances chimiques
Myostatin
0
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
0
Ppargc1a protein, rat
0
RNA, Messenger
0
Reactive Oxygen Species
0
Hydrogen Peroxide
BBX060AN9V
PCSK9 protein, rat
EC 3.4.21.-
Proprotein Convertase 9
EC 3.4.21.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Università degli Studi di Genova
ID : 100010-2016-BP-FRA_001
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