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MicroRNA-30e targets BNIP3L to protect against aldosterone-induced podocyte apoptosis and mitochondrial dysfunction
Yan Guo1,2, Xu Deng1,2, Shuang Chen1,2
1Department of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing, China; and.
Abstract:
MicroRNAs are essential for the maintenance of podocyte homeostasis. Emerging evidence has demonstrated a protective role of microRNA-30a (miR-30a), a member of the miR-30 family, in podocyte injury. However, the roles of other miR-30 family members in podocyte injury are unclear. The present study was undertaken to investigate the contribution of miR-30e to the pathogenesis of podocyte injury induced by aldosterone (Aldo), as well as the underlying mechanism. After Aldo treatment, miR-30e was reduced in a dose-and time-dependent manner. Notably, overexpression of miR-30e markedly attenuated Aldo-induced apoptosis in podocytes. In agreement with this finding, miR-30e silencing led to significant podocyte apoptosis. Mitochondrial dysfunction (MtD) has been shown to be an early event in Aldo-induced podocyte injury. Here we found that overexpression of miR-30e improved Aldo-induced MtD while miR-30e silencing resulted in MtD. Next, we found that miR-30e could directly target the BCL2/adenovirus E1B-interacting protein 3-like (BNIP3L) gene. Aldo markedly enhanced BNIP3L expression in podocytes, and silencing of BNIP3L largely abolished Aldo-induced MtD and cell apoptosis. On the contrary, overexpression of BNIP3L induced MtD and apoptosis in podocytes. Together, these findings demonstrate that miR-30e protects mitochondria and podocytes from Aldo challenge by targeting BNIP3L.
Insights
MicroRNA-30e (miR-30e) protects kidney podocytes from aldosterone-induced injury. It prevents mitochondrial dysfunction and apoptosis by targeting the BNIP3L gene, offering a potential therapeutic target for kidney disease.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- MicroRNAs regulate podocyte homeostasis and injury.
- MicroRNA-30a shows protective effects, but other family members' roles are unknown.
- Aldosterone induces podocyte injury, involving mitochondrial dysfunction.
Purpose of the Study:
- Investigate miR-30e's role in aldosterone-induced podocyte injury.
- Elucidate the underlying molecular mechanism involving BNIP3L.
Main Methods:
- Aldosterone treatment of podocytes.
- Overexpression and silencing of miR-30e and BNIP3L.
- Assessment of apoptosis and mitochondrial dysfunction.
- Gene target analysis using luciferase assay.
Main Results:
- Aldosterone reduced miR-30e levels in a dose- and time-dependent manner.
- miR-30e overexpression attenuated aldosterone-induced apoptosis and mitochondrial dysfunction.
- miR-30e directly targets BNIP3L, which mediates aldosterone-induced podocyte injury.
Conclusions:
- miR-30e protects podocytes from aldosterone-induced injury.
- This protection is achieved by targeting BNIP3L and ameliorating mitochondrial dysfunction.
- miR-30e represents a potential therapeutic target for kidney diseases involving aldosterone-induced podocyte damage.
