MiR-454-3p regulates high glucose-induced mesothelial-mesenchymal transition and glycolysis in peritoneal mesothelial cells by targeting STAT3.
MicroRNAs
/ metabolism
STAT3 Transcription Factor
/ metabolism
Humans
Epithelial-Mesenchymal Transition
/ drug effects
Glucose
/ metabolism
Glycolysis
/ drug effects
Peritoneal Dialysis
/ adverse effects
Peritoneal Fibrosis
/ metabolism
Peritoneum
/ pathology
Male
Female
Middle Aged
Cell Line
Down-Regulation
Epithelial Cells
/ metabolism
Glycolysis
STAT3
mesothelial-mesenchymal transition (MMT)
miR-454-3p
peritoneal fibrosis
Journal
Renal failure
ISSN: 1525-6049
Titre abrégé: Ren Fail
Pays: England
ID NLM: 8701128
Informations de publication
Date de publication:
Dec 2024
Dec 2024
Historique:
medline:
28
8
2024
pubmed:
28
8
2024
entrez:
28
8
2024
Statut:
ppublish
Résumé
The quality of life of patients receiving long-term peritoneal dialysis (PD) is significantly impacted by the onset of peritoneal fibrosis (PF), and one of the pathological changes is mesothelial-mesenchymal transition (MMT). In this study, we investigated the potential roles of miR-454-3p and signal transducer and activator of transcription 3 (STAT3) in the progression of peritoneal MMT and the underlying mechanisms. Peritoneums were collected to detect morphology MiR-454-3p was downregulated in the peritoneums and PD effluent-derived cell populations of long-term PD patients. High glucose (HG) treatment promoted HMrSV5 cell MMT and glycolysis. MiR-454-3p overexpression alleviated HG-induced MMT and suppressed the expression of STAT3 and glycolytic enzymes. In contrast, the miR-454-3p inhibitor exacerbated HG-induced MMT and promoted the expression of glycolytic enzymes and STAT3. Moreover, STAT3 was the target of miR-454-3p. This study demonstrated the protective role of miR-454-3p in HG-induced MMT and glycolysis in HMrSv5 cells, suggesting that miR-454-3p may prevent MMT by suppressing glycolytic enzymes
Sections du résumé
BACKGROUND
UNASSIGNED
The quality of life of patients receiving long-term peritoneal dialysis (PD) is significantly impacted by the onset of peritoneal fibrosis (PF), and one of the pathological changes is mesothelial-mesenchymal transition (MMT). In this study, we investigated the potential roles of miR-454-3p and signal transducer and activator of transcription 3 (STAT3) in the progression of peritoneal MMT and the underlying mechanisms.
METHODS
UNASSIGNED
Peritoneums were collected to detect morphology
RESULTS
UNASSIGNED
MiR-454-3p was downregulated in the peritoneums and PD effluent-derived cell populations of long-term PD patients. High glucose (HG) treatment promoted HMrSV5 cell MMT and glycolysis. MiR-454-3p overexpression alleviated HG-induced MMT and suppressed the expression of STAT3 and glycolytic enzymes. In contrast, the miR-454-3p inhibitor exacerbated HG-induced MMT and promoted the expression of glycolytic enzymes and STAT3. Moreover, STAT3 was the target of miR-454-3p.
CONCLUSIONS
UNASSIGNED
This study demonstrated the protective role of miR-454-3p in HG-induced MMT and glycolysis in HMrSv5 cells, suggesting that miR-454-3p may prevent MMT by suppressing glycolytic enzymes
Identifiants
pubmed: 39192609
doi: 10.1080/0886022X.2024.2394635
doi:
Substances chimiques
MicroRNAs
0
STAT3 Transcription Factor
0
STAT3 protein, human
0
Glucose
IY9XDZ35W2
MIRN454 microRNA, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM