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Updated: Apr 5, 2026

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli
Published on: June 27, 2015
Cabin1 localizes in glomerular podocyte and undergoes nuclear translocation during podocyte injury
Yueqiang Wen1, Zebin Wang1, Lingling Liu2
1a Department of Nephrology , The Second Affiliated Hospital, GuangZhou Medical University , Guangzhou , China and.
Context:
Podocyte injury is related to increasing proteinuria and contributes to the progression of kidney disease. Calcineurin binding protein 1 (Cabin1) is a repressor of myocyte enhancer factor 2 (MEF2) and calcineurin-mediated transcription in the immune system. Moreover, Cabin1 interacts with p53 and negatively regulates p53 in tumor cells. However, its function in kidney is unknown.
Objective:
To explore the exact localization of Cabin1 in glomeruli, as well as the relationship between Cabin1 and podocyte injury.
Methods:
Sprague-Dawley rats were sacrificed to observe the localization and protein expression of Cabin1 in the kidney. Cabin1 localization and protein expression were detected by immunofluorescence staining and western blot, respectively. Mouse podocytes were cultivated at 33 °C to propagate, then cells were transferred to an incubator at 37 °C to allow differentiation. Differentiated podocytes were stimulated by angiotensin II (AngII) or AngII plus tacrolimus. Cells were harvested to detect the localization and protein expression of Cabin1. Cytoplasmic and nuclear protein were separated by protein extraction kit.
Results:
Cabin1 mainly localized in the nuclei of glomerular innate cells, it colocalized with WT-1 in podocytes nuclei. Western bolt showed Cabin1 protein remarkably expressed in renal cortex. AngII-induced Cabin1 nuclear protein significantly increased, accompanied by cytoskeleton disruption in cultured mouse podocytes.
Conclusion:
Cabin1 localizes in glomerular podocytes. AngII induces nuclear translocation of Cabin1 in cultured podocytes.
Insights
Calcineurin binding protein 1 (Cabin1) is found in kidney podocytes. Angiotensin II (AngII) increases Cabin1 in podocyte nuclei, potentially linking it to kidney disease progression.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Podocyte injury is a key factor in progressive kidney disease and proteinuria.
- Calcineurin binding protein 1 (Cabin1) is known to regulate transcription in immune and tumor cells, but its role in the kidney is uncharacterized.
Purpose of the Study:
- To determine the precise localization of Cabin1 within the glomerulus.
- To investigate the association between Cabin1 expression and podocyte injury.
Main Methods:
- Immunofluorescence staining and Western blot were used to analyze Cabin1 localization and expression in rat kidneys.
- Cultured mouse podocytes were stimulated with angiotensin II (AngII) with or without tacrolimus to assess Cabin1's response.
Main Results:
- Cabin1 was primarily detected in the nuclei of glomerular cells, co-localizing with WT-1 in podocyte nuclei.
- Western blot confirmed significant Cabin1 expression in the renal cortex.
- AngII stimulation led to a notable increase in nuclear Cabin1 and induced cytoskeleton disruption in podocytes.
Conclusions:
- Cabin1 is localized within glomerular podocytes.
- Angiotensin II promotes the nuclear translocation of Cabin1 in cultured podocytes, suggesting a role in podocyte function and injury.
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