This study investigates the role of the proteasome in maintaining kidney filtration barrier integrity by modulating endocytosis in glomerular cells. The research explores how proteasomal activity in podocytes and glomerular endothelial cells affects endocytic processes essential for kidney function.
Endothelial cell-specific deletion of β5i led to morphological alterations in the glomerular filtration barrier, including loss of endothelial fenestrations and podocyte foot process effacement. These structural changes were associated with impaired endocytic activity, resulting in proteinuria and glomerular immunoglobulin deposition.
The study utilized a tamoxifen-inducible, endothelial cell-specific Lmp7 (β5i) Knockout mouse model. This model was generated by crossing mice expressing Cre recombinase under an endothelial-specific promoter with mice harboring floxed Lmp7 alleles, allowing for conditional deletion of the immunoproteasome subunit β5i in endothelial cells upon tamoxifen administration.
Nephrology, Glomerular filtration, Endocytosis, Proteasome function, Kidney disease
Tamoxifen-inducible Knockout, Endothelial cell-specific deletion, Cre-loxP system, Immunoproteasome, Glomerular endothelial cells
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