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MiR-133 inhibits kidney injury in rats with diabetic nephropathy via MAPK/ERK pathway
1Department of Nephrology, Suzhou Kowloon Hospital, Medical School of Shanghai Jiaotong University, Suzhou, China. 385534405@qq.com.
Objective:
The aim of this study was to explore the effect of micro ribonucleic acid (miR)-133 on kidney injury in rats with diabetic nephropathy (DN) through the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway.
Materials And Methods:
The model of DN was first established in rats. Blood glucose, renal index, urinary micro-albumin (UMA), and creatinine clearance rate (CCr) were detected. Meanwhile, the protein expression levels of miR-133, kidney injury molecule-1 (KIM-1) and anti-inflammatory cytokine interleukin-8 (IL-8) were measured using Western blotting. Human renal proximal tubular epithelial cell line human kidney-2 (HK-2) was treated with high glucose to simulate DN cells in vivo. Subsequently, Western blotting was performed to detect the protein expression of KIM-1. After HK-2 cells were treated with high glucose and silenced miR-133 for 24 h, the expression changes in KIM-1 was evaluated.
Results:
In DN group, blood glucose, renal index, UMA, and CCr were all markedly higher than those of control group. This indicated the successful establishment of DN model in rats. The expression level of miR-133 was significantly up-regulated in DN model rats. Meanwhile, the downstream protein phosphorylated-EPK (p-EPK) showed a significantly increasing trend as well. Additionally, the protein expressions of KIM-1 and IL-8 were notably elevated. High-glucose-treated HK-2 cells showed significantly up-regulated expression levels of miR-133, KIM-1, and IL-8. After 24 h of combined treatment with high glucose and miR-133 silence, the expressions of KIM-1 and IL-8 were markedly down-regulated.
Conclusions:
MiR-133 may be related to the occurrence and development of DN. The silence of miR-133 inhibits kidney injury in DN via the MAPK/ERK signaling pathway. Our findings suggest that miR-133 may be an effective target for the treatment of DN.
Insights
Micro ribonucleic acid (miR)-133 is linked to kidney injury in diabetic nephropathy (DN). Silencing miR-133 can inhibit kidney damage by affecting the MAPK/ERK pathway, suggesting it as a potential therapeutic target for DN.
Area of Science:
- Biochemistry
- Molecular Biology
- Nephrology
Background:
- Diabetic nephropathy (DN) is a major complication of diabetes, characterized by progressive kidney damage.
- Micro ribonucleic acid (miR)-133 is implicated in various cellular processes, but its role in DN remains unclear.
Purpose of the Study:
- To investigate the effect of miR-133 on kidney injury in a rat model of diabetic nephropathy (DN).
- To explore the underlying mechanism involving the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway.
Main Methods:
- Established a DN rat model and assessed key indicators like blood glucose, renal index, urinary micro-albumin (UMA), and creatinine clearance rate (CCr).
- Utilized Western blotting to measure protein expression of miR-133, kidney injury molecule-1 (KIM-1), and interleukin-8 (IL-8).
- Used high-glucose-treated human kidney-2 (HK-2) cells to simulate DN in vitro, evaluating miR-133 and KIM-1 expression changes after miR-133 silencing.
Main Results:
- DN model rats exhibited significantly elevated blood glucose, renal index, UMA, and CCr compared to controls.
- miR-133 expression and phosphorylated-ERK (p-ERK) levels were significantly increased in DN rats and high-glucose-treated HK-2 cells.
- Expressions of KIM-1 and IL-8 were notably elevated in DN models, and silencing miR-133 reduced KIM-1 and IL-8 levels in vitro.
Conclusions:
- miR-133 plays a role in the development of diabetic nephropathy.
- Inhibition of kidney injury in DN by silencing miR-133 occurs via the MAPK/ERK signaling pathway.
- miR-133 represents a promising therapeutic target for managing diabetic nephropathy.
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