Constitutional Nephrin Deficiency in Conditionally Immortalized Human Podocytes Induced Epithelial-Mesenchymal Transition, Supported by -Catenin/NF-kappa B Activation: A Consequence of Cell Junction Impairment?
Figure 9
Nephrin and -SMA expression in kidney biopsies from a normal individual and a patient carrying a Finnish mutation p.S569R (c.1707CA) (NPHS1) and in IgAN. Immunofluorescence and confocal analysis were carried out as described in Section 2. (A) Nephrin expression in normal (WT) (a) and NPHS1 kidney (b). (c) shows the antibody negative control. (B) Negative control for -SMA (a) expression and WT1 (b) antibodies and their merged signals (d). (C) -SMA and WT1 expression in normal (WT) and NPHS1 kidney (WT a-b and p.S569R d-e) and their merged signal (c-f). -SMA colocalizes with WT1 indicating its podocyte origin. (D) Enlarged particular of panel (c) showing the colocalization of -SMA and WT1 in NPHS1 kidney tissue and their merged signals (a, b, and c). (E) -SMA expression in healthy or IgA nephropaty (IgAN) renal biopsy. The technical details are described in Section 2. The figure shows a typical experiment of at least three performed under the same conditions.
