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MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23
Diabetic nephropathy (DN) remains the major cause of end‐stage renal disease. MicroRNAs (miRNAs) have been reported to perform biological functions in many diseases. This investigation elucidated the biological role of miR‐17‐5p in DN. In this study, high glucose‐cultured human mesangial cells (HMCs) were used as a cell model of DN. The miR‐17‐5p and KIF23 expression was measured by RT‐qPCR. Cell apoptosis was detected by flow cytometry. The protein levels of apoptosis markers, fibrosis markers, and Wnt/β‐catenin signaling‐related genes were assessed using western blotting. The interaction of miR‐17‐5p with KIF23 was tested by a luciferase reporter assay. We found that miR‐17‐5p was upregulated in both DN patients and high glucose‐treated HMCs. Silencing miR‐17‐5p attenuated the apoptosis and fibrosis in high glucose‐treated HMCs. MiR‐17‐5p binds to KIF23 3′UTR and negatively regulates KIF23 expression. KIF23 knockdown could suppress the role of miR‐17‐5p inhibition in high glucose‐treated HMCs. Additionally, inhibition of miR‐17‐5p activated Wnt/β‐catenin signaling in HMCs through upregulating KIF23 expression. Suppression of Wnt/β‐catenin signaling antagonized the effect of miR‐17‐5p in HMCs. In conclusion, miR‐17‐5p inhibition alleviates the apoptosis and fibrosis in high glucose‐treated HMCs by targeting KIF23 activating Wnt/β‐catenin signaling.
MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23
Diabetic nephropathy (DN) remains the major cause of end‐stage renal disease. MicroRNAs (miRNAs) have been reported to perform biological functions in many diseases. This investigation elucidated the biological role of miR‐17‐5p in DN. In this study, high glucose‐cultured human mesangial cells (HMCs) were used as a cell model of DN. The miR‐17‐5p and KIF23 expression was measured by RT‐qPCR. Cell apoptosis was detected by flow cytometry. The protein levels of apoptosis markers, fibrosis markers, and Wnt/β‐catenin signaling‐related genes were assessed using western blotting. The interaction of miR‐17‐5p with KIF23 was tested by a luciferase reporter assay. We found that miR‐17‐5p was upregulated in both DN patients and high glucose‐treated HMCs. Silencing miR‐17‐5p attenuated the apoptosis and fibrosis in high glucose‐treated HMCs. MiR‐17‐5p binds to KIF23 3′UTR and negatively regulates KIF23 expression. KIF23 knockdown could suppress the role of miR‐17‐5p inhibition in high glucose‐treated HMCs. Additionally, inhibition of miR‐17‐5p activated Wnt/β‐catenin signaling in HMCs through upregulating KIF23 expression. Suppression of Wnt/β‐catenin signaling antagonized the effect of miR‐17‐5p in HMCs. In conclusion, miR‐17‐5p inhibition alleviates the apoptosis and fibrosis in high glucose‐treated HMCs by targeting KIF23 activating Wnt/β‐catenin signaling.
MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23
Chen, Xiaoli (author) / Gu, Liyan (author) / Cheng, Xia (author) / Xing, Jianping (author) / Zhang, Minxia (author)
Environmental Toxicology ; 36 ; 1702-1712
2021-08-01
11 pages
Article (Journal)
Electronic Resource
English
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