Upregulation of miRNA-1228-3p alleviates TGF-β-induced fibrosis in renal tubular epithelial cells.
Bone Morphogenetic Proteins
/ genetics
Cell Line
Epithelial Cells
/ drug effects
Fibrosis
Growth Differentiation Factors
/ genetics
Humans
Kidney Tubules, Proximal
/ drug effects
MicroRNAs
/ genetics
Signal Transduction
Smad2 Protein
/ genetics
Smad4 Protein
/ genetics
Transforming Growth Factor beta1
/ toxicity
Up-Regulation
Journal
Histology and histopathology
ISSN: 1699-5848
Titre abrégé: Histol Histopathol
Pays: Spain
ID NLM: 8609357
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
pubmed:
29
7
2020
medline:
2
10
2021
entrez:
29
7
2020
Statut:
ppublish
Résumé
Chronic kidney disease (CKD) has become a major public health issue, which can lead to renal fibrosis regardless of the initial injury. It has been previously reported that miRNA-1228-3p was correlate with the progression of kidney fibrosis. However, the mechanism by which miRNA-1228-3p regulates renal fibrosis remains unclear. Renal tubular epithelial cells (HK-2) were treated with TGF-β1 (10 ng/ml) in an in vitro model of renal fibrosis. Gene and protein expressions in HK-2 cells were measured by Western-blot and RT-qPCR, respectively. The relation between miRNA-1228-3p and its target gene was investigated by dual luciferase report analysis. Upregulation of miRNA-1228-3p significantly inhibited TGF-β1-induced fibrosis of HK-2 cells in vitro by targeting GDF11. In addition, miRNA-1228-3p exhibited anti-fibrosis effect through inhibition of the smad2/smad4 signaling pathway. Upregulation of miRNA-1228-3p markedly inhibited the progression of renal fibrosis in vitro, indicating that miRNA-1228-3p may serve as a potential novel target for the treatment of renal fibrosis.
Sections du résumé
BACKGROUND
BACKGROUND
Chronic kidney disease (CKD) has become a major public health issue, which can lead to renal fibrosis regardless of the initial injury. It has been previously reported that miRNA-1228-3p was correlate with the progression of kidney fibrosis. However, the mechanism by which miRNA-1228-3p regulates renal fibrosis remains unclear.
METHODS
METHODS
Renal tubular epithelial cells (HK-2) were treated with TGF-β1 (10 ng/ml) in an in vitro model of renal fibrosis. Gene and protein expressions in HK-2 cells were measured by Western-blot and RT-qPCR, respectively. The relation between miRNA-1228-3p and its target gene was investigated by dual luciferase report analysis.
RESULTS
RESULTS
Upregulation of miRNA-1228-3p significantly inhibited TGF-β1-induced fibrosis of HK-2 cells in vitro by targeting GDF11. In addition, miRNA-1228-3p exhibited anti-fibrosis effect through inhibition of the smad2/smad4 signaling pathway.
CONCLUSION
CONCLUSIONS
Upregulation of miRNA-1228-3p markedly inhibited the progression of renal fibrosis in vitro, indicating that miRNA-1228-3p may serve as a potential novel target for the treatment of renal fibrosis.
Identifiants
pubmed: 32720699
pii: HH-18-242
doi: 10.14670/HH-18-242
doi:
Substances chimiques
Bone Morphogenetic Proteins
0
GDF11 protein, human
0
Growth Differentiation Factors
0
MIRN1228 microRNA, human
0
MicroRNAs
0
SMAD2 protein, human
0
SMAD4 protein, human
0
Smad2 Protein
0
Smad4 Protein
0
Transforming Growth Factor beta1
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1125-1133Subventions
Organisme : Construction of Home-management System for Hemodialysis Patients Based on Internet of Things and Large Data Platform
ID : LGF19H050005
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