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Updated: Oct 16, 2025

An Efficient Sieving Method to Isolate Intact Glomeruli from Adult Rat Kidney

An Efficient Sieving Method to Isolate Intact Glomeruli from Adult Rat Kidney

Published on: November 1, 2018

Podocyte-specific Crb2 knockout mice develop focal segmental glomerulosclerosis.

Akiko Tanoue¹, Kan Katayama^2,3, Yugo Ito^4,5

¹Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.

Scientific Reports

|October 16, 2021

Summary

Loss of cell polarity protein Crb2 in kidney podocytes causes focal segmental glomerulosclerosis. This protein deficiency leads to podocyte injury, apoptosis, and impaired kidney function, highlighting its critical role in glomerular health.

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Assessment of Kidney Function in Mouse Models of Glomerular Disease

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Last Updated: Oct 16, 2025

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Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

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Assessment of Kidney Function in Mouse Models of Glomerular Disease

Assessment of Kidney Function in Mouse Models of Glomerular Disease

Published on: June 30, 2018

Area of Science:

Nephrology
Cell Biology
Molecular Medicine

Background:

Crumbs homologue 2 (Crb2) is a cell polarity protein crucial for kidney podocyte function.
Mutations in CRB2 are linked to steroid-resistant nephrotic syndrome, but the underlying mechanisms remain unclear.

Purpose of the Study:

To investigate the role of podocyte-specific Crb2 in the development of kidney disease.
To elucidate the cellular and molecular mechanisms by which Crb2 deficiency leads to podocyte dysfunction and glomerulosclerosis.

Main Methods:

Generation and analysis of podocyte-specific Crb2 knockout mice.
Assessment of kidney function through urinalysis (albuminuria, microhematuria).
Histopathological examination including electron microscopy and immunohistochemistry for podocyte markers (Wt1, Nphs2, Podxl, Nphs1).
In vitro studies on human podocytes lacking CRB2 to assess F-actin organization and apoptosis.

Main Results:

Podocyte-specific Crb2 knockout mice exhibited massive albuminuria and microhematuria by 2 months, progressing to focal segmental glomerulosclerosis and tubulointerstitial fibrosis by 6 months.
Electron microscopy revealed podocyte injury and foot process effacement in knockout mice.
Reduced glomerular Wt1-positive cells and decreased expression of key podocyte markers (Nphs2, Podxl, Nphs1) were observed.
Human podocytes lacking CRB2 showed reduced F-actin area and increased susceptibility to apoptosis.

Conclusions:

Podocyte-specific Crb2 deficiency induces significant alterations in the actin cytoskeleton, leading to podocyte dysfunction and apoptosis.
These cellular changes ultimately result in the development of focal segmental glomerulosclerosis.
Crb2 is essential for maintaining podocyte integrity and preventing glomerular disease.