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Stimulation of miRNA-1906 restores podocyte function in ischemia-induced renal injury by restoring SLIT2/ROBO1 signalling pathway |
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| รหัสดีโอไอ | |
| Creator | Zhiheng Ma |
| Title | Stimulation of miRNA-1906 restores podocyte function in ischemia-induced renal injury by restoring SLIT2/ROBO1 signalling pathway |
| Contributor | Jiping Qin, Sanbin Xu, Meiqin Huang |
| Publisher | Maejo University |
| Publication Year | 2568 |
| Journal Title | Maejo International Journal of Science and Technology |
| Journal Vol. | 19 |
| Journal No. | 2 |
| Page no. | 196 |
| Keyword | miRNA-1906 agomir, podocyte, kidney injury, ischemia, reperfusion, SLIT2/ROBO1 pathway |
| Website title | Maejo International Journal of Science and Technology |
| ISSN | 1905-7873 |
| Abstract | The present study evaluates the nephroprotective effect and molecular function of miRNA-1906 stimulation on ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) in mice. Clamping kidney tissues caused I/R-induced renal injury. In this study, 18 mice were divided into three distinct groups (n = 6): control group, AKI group and miRNA-1906 agomir Test group. The miRNA-1906 group received 500 nmol/kg of miRNA-1906 agomir administered intrathecally for 24 hrs before the induction of ischemia. The effects of miRNA-1906 stimulation on kidney function, oxidative stress and mediators of inflammation were evaluated. The expressions of Slit Guidance Ligand 2 (SLIT2), Roundabout homolog 1 (ROBO1), desmin, caspase-3, Transient Receptor Potential Canonical 6 (TRPC6), phosphorylated Akt (p-Akt) and nephrin in renal tissues were measured by western blot to investigate the impact of miRNA-1906 stimulation on podocyte damage. Histopathological changes were assessed with hematoxylin and eosin staining. The miRNA-1906 agomir reduced the serum levels of creatinine and blood urea nitrogen, as well as the excretion of microalbumin, in the AKI group. The treatment with miRNA-1906 agomir also lowered levels of oxidative stress and inflammatory mediators in the kidney tissues of mice that I/R had injured. In comparison to the AKI group, the miRNA-1906 agomir treatment also resulted in a notable upregulation of desmin, caspase-3, and Transient Receptor Potential Cation Channel 6 (TRPC-6), as well as a significant reduction in nephrin. The miRNA-1906 agomir also reduced SLIT2/ROBO1 circuit modification, restoring podocyte function. The I/R-induced AKI was resolved by stimulating miRNA-1906 with miRNA-1906 agomir. This controls podocyte damage by blocking the SLIT2/ROBO1 pathway. |
