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Published on: November 30, 2013
MicroRNA-30/Cx43 axis contributes to podocyte injury by regulating ER stress in diabetic nephropathy
Min Li1, Weijie Ni2, Mengyu Zhang1
1Department of Nephrology, the Third Affiliated Hospital of Soochow University, Changzhou, China.
Background:
The microRNA-30 family plays a critical role in the pathogenesis of podocyte injury. Cx43 plays an essential role in intercellular communication, which is essential for coordinated kidney function. This study was conducted to explore the function of microRNA-30s/Cx43 in podocyte injury in diabetic nephropathy (DN), both in vivo and in vitro.
Methods:
SD rats were given streptozotocin (STZ) injections to induce DN. Podocytes were incubated in the medium in the presence or absence of high glucose (HG). The effects of the microRNA-30/Cx43 axis on DN and its underlying mechanisms were investigated by TUNEL assay, PAS, immunohistochemical staining, immunofluorescence staining, Western blot, RT-qPCR, RNA interference, and luciferase reporter assay. Podocytes were transfected with microRNA-30 family mimics, microRNA-30 family inhibitors, Cx43 siRNA, and negative controls to detect the effect of the microRNA-30/Cx43 axis. MicroRNA-30 family mimic AAVs, and microRNA-30 family inhibitor AAVs applied to regulate microRNA-30 family expression in the kidneys of the STZ-induced DN model rats to reveal the underlying mechanisms of the microRNA-30/Cx43 axis in DN.
Results:
MicroRNA-30 family member expression was downregulated in HG-treated podocytes and the glomeruli of STZ-induced DN rats. Luciferase reporter assays confirmed Cx43 is a directed target of microRNA-30s. The overexpression of microRNA-30 family members attenuated the HG-induced podocyte injury and protected against podocyte apoptosis and endoplasmic reticulum stress (ERS) both in vivo and in vitro. Also, silencing Cx43 expression eased podocyte apoptosis, injury, and ERS induced by a HG+microRNA-30 family inhibitor. Double-immunofluorescence staining assays proved the co-localization of caspase12 and Cx43.
Conclusions:
The overexpression of microRNA-30 family members prevents HG-induced podocyte injury and attenuates ERS by modulating Cx43 expression. The microRNA-30/Cx43/ERS axis might be a potential therapeutic target to treat DN.
Insights
MicroRNA-30 family members protect against diabetic nephropathy (DN) podocyte injury by targeting Cx43. Upregulating microRNA-30s attenuates endoplasmic reticulum stress (ERS) and podocyte damage in DN, suggesting a therapeutic target.
Area of Science:
- Molecular Biology
- Nephrology
- Cell Biology
Background:
- The microRNA-30 family is crucial in podocyte injury pathogenesis.
- Connexin-43 (Cx43) is vital for intercellular communication in kidney function.
- This study investigates the microRNA-30s/Cx43 axis in diabetic nephropathy (DN) podocyte injury.
Purpose of the Study:
- To explore the role of the microRNA-30/Cx43 axis in podocyte injury within diabetic nephropathy.
- To elucidate the underlying mechanisms of this axis in DN progression.
- To evaluate the therapeutic potential of targeting the microRNA-30/Cx43/Endoplasmic Reticulum Stress (ERS) axis.
Main Methods:
- Diabetic nephropathy (DN) was induced in Sprague-Dawley (SD) rats using streptozotocin (STZ).
- Podocytes were cultured under high glucose (HG) conditions.
- Techniques included TUNEL assay, PAS staining, immunohistochemistry, immunofluorescence, Western blot, RT-qPCR, RNA interference, and luciferase reporter assays. Adeno-associated viruses (AAVs) were used to modulate microRNA-30 family expression in vivo.
Main Results:
- MicroRNA-30 family expression was reduced in HG-treated podocytes and DN rat glomeruli.
- Cx43 was confirmed as a direct target of microRNA-30s.
- Overexpression of microRNA-30 family members attenuated HG-induced podocyte injury, apoptosis, and endoplasmic reticulum stress (ERS) both in vivo and in vitro. Silencing Cx43 also eased HG+microRNA-30 inhibitor-induced podocyte damage and ERS.
Conclusions:
- Overexpression of microRNA-30 family members prevents high glucose-induced podocyte injury and attenuates endoplasmic reticulum stress (ERS) by modulating Cx43 expression.
- The microRNA-30/Cx43/ERS axis represents a potential therapeutic target for treating diabetic nephropathy (DN).
- Co-localization of caspase-12 and Cx43 was observed, suggesting a link to ERS pathways.
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