miR-34b-3p protects against acute kidney injury in sepsis mice via targeting ubiquitin-like protein 4A.
AKI
NF-κB
UBL4A
miR-34b-3p
sepsis
Journal
The Kaohsiung journal of medical sciences
ISSN: 2410-8650
Titre abrégé: Kaohsiung J Med Sci
Pays: China (Republic : 1949- )
ID NLM: 100960562
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
received:
20
04
2020
revised:
25
05
2020
accepted:
02
06
2020
pubmed:
2
7
2020
medline:
3
8
2021
entrez:
2
7
2020
Statut:
ppublish
Résumé
MicroRNAs (miRNAs) have been reported as a diagnostic markers for sepsis, and miRNAs have also been found to play a regulatory role in sepsis-induced acute kidney injury (AKI). However, the regulatory effect and mechanism of miR-34b-3p on AKI remains elusive. First, sepsis mice with AKI was established via cecal ligation puncture (CLP), and verified through hematoxylin-eosin staining, determination of tumor necrosis factor-α (TNF-α), interleukin (IL)-6/1β and serum levels of alanine aminotransferase (ALT) and blood urea nitrogen (BUN). Data showed that CLP-induced mice demonstrated increased ALT, BUN, TNF-α, IL-1β, and IL-6 with injured pathological morphology of kidney tissues. Second, lipopolysaccharide (LPS) treatment elevated TNF-α, IL-1β, and IL-6 contents in rat mesangial cells (RMCs). MiR-34b-3p was downregulated in both CLP-induced mice and LPS-induced RMCs. Third, target gene of miR-34b-3p was verified as ubiquitin-like protein 4A (UBL4A), and UBL4A was upregulated in LPS-induced RMCs. MiR-34b-3p could inhibit UBL4A expression and decreased TNF-α, IL-1β and IL-6 contents in LPS-induced RMCs, while overexpression of UBL4A counteract with the suppressive effects of miR-34b-3p on the protein expression. Moreover, transcriptional activity of UBL4A-induced NF-κB was decreased by miR-34b-3p. Lastly, in vivo injection of miR-34b-3p agomir improved CLP-induced kidney tissues injury with declined ALT, BUN, TNF-α, IL-1β, IL-6, and UBL4A. In general, miR-34b-3p overexpression could alleviate AKI in sepsis mice through downregulation of UBL4A/NF-κB, providing potential therapeutic strategy for AKI.
Substances chimiques
MIRN34b microRNA, mouse
0
MicroRNAs
0
Ubiquitins
0
Ubl4a protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
817-824Informations de copyright
© 2020 The Authors. The Kaohsiung Journal of Medical Sciences published by John Wiley & Sons Australia on behalf of Kaohsiung Medical University.
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