Influence of renal ischaemia-reperfusion injury on renal neutrophil gelatinase-associated lipocalin receptor (24p3R) in rats.
24p3R
ischaemia-reperfusion
kidney injury
megalin
neutrophil gelatinase-associated lipocalin
Journal
Clinical and experimental pharmacology & physiology
ISSN: 1440-1681
Titre abrégé: Clin Exp Pharmacol Physiol
Pays: Australia
ID NLM: 0425076
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
12
06
2018
revised:
02
06
2019
accepted:
13
06
2019
pubmed:
19
6
2019
medline:
29
8
2020
entrez:
19
6
2019
Statut:
ppublish
Résumé
The neutrophil gelatinase-associated lipocalin (NGAL) receptor (24p3R) is expressed in distal nephron and contributes to the endocytosis of NGAL in urine. This study was undertaken to evaluate an influence of renal ischaemia-reperfusion injury on 24p3R. Unilateral renal pedicle was clamped for 0, 10, 20, 30, or 45 minutes in male Wistar rats. Urine was collected for 24 hours after reperfusion, and ischaemic kidney and blood sample were obtained. Apparent histological injury in the ischaemic kidney was detected in the 30 and 45 minutes-treated groups. Urinary NGAL excretion elevated in rats with renal ischaemia for more than 20 minutes, while serum creatinine increased in rats for more than 30 minutes of ischaemia. Renal protein expression of NGAL did not significantly change. Renal mRNA expressions of megalin and cubilin, which are expressed at renal proximal tubules and uptake NGAL, decreased in animals with renal ischaemia for more than 20 minutes. Renal protein expression of 24p3R, which is expressed at renal distal tubules and uptake NGAL, decreased in rats with renal ischaemia for 45 min. This study showed for the first time that renal 24p3R decreased in response to renal ischaemia. As relatively longer renal ischaemia (45 minutes) decreased renal 24p3R protein and increased urinary NGAL excretion, the down-regulation of 24p3R protein might contribute to the elevated urinary excretion of NGAL in rats with unilateral ischaemia-reperfusion injury.
Identifiants
pubmed: 31211866
doi: 10.1111/1440-1681.13129
doi:
Substances chimiques
24p3R receptor, rat
0
Biomarkers
0
Lcn2 protein, rat
0
Lipocalin-2
0
Receptors, Cell Surface
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1166-1173Informations de copyright
© 2019 John Wiley & Sons Australia, Ltd.
Références
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