In:
Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-1-27), p. 1-17
Abstract:
Aim. The study is aimed at verifying miR-154-5p and Smurf1 combination in glomerular mesangial cells regulating TGFβ1/Smad3 pathway-related protein ubiquitination in the model of diabetic rats renal tissues, primary mesangial cells, and cell lines. Methods. The diabetic SD rat model and high-glucose-cultured primary mesangial cells and cell lines were established. miR-154-5p mimic and inhibitor, Smurf1 siRNA, and TGF β 1/Smad3 inhibitor (SB431542) were pretreated to make the TGFβ1/Smad3 pathway and ubiquitin changes. Fluorescence in situ hybridization was used for the miR-154-5p renal localization; molecular biological detection was adopted for cell proliferation, renal function, urine protein, and pathway proteins. After bioinformatics predicted binding sites, luciferase and Co-IP were used to detect miRNA and protein binding. Results. miR-154-5p was significantly increased and mainly concentrated in the glomerular of renal cortex in well-established diabetic rat renal tissues. Rno-miR-154-5p combined Rno-Smurf1 3 ′ UTR, while Smurf1 combined Smad3 directly. Meanwhile, miR-154-5p regulates TGFβ1/Smad3-mediated cell proliferation via Smurf1 ubiquitination. Conclusion. miR-154-5p regulates the TGFβ1/Smads pathway through Smurf1 ubiquitination and promotes the fibrosis process of diabetic kidney disease.
Type of Medium:
Online Resource
ISSN:
1942-0994
,
1942-0900
DOI:
10.1155/2022/7502632
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2022
detail.hit.zdb_id:
2455981-7
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