Cadherin and catenin staining in podocytes in development and puromycin aminonucleoside nephrosis

Abstract

Podocytes have been shown to express classical cadherins in the early stage of glomerulogenesis, but it remains unclear whether podocytes in normal and pathological conditions express cadherins in the adult stage. To address this question, rat podocytes in the neonate, the adult and in puromycin aminonucleoside (PAN) nephrosis were examined by immunofluorescence microscopy using antibodies against alpha- and beta-catenins and anti-pan-cadherin antibody, and by immunoelectron microscopy using anti-alpha-catenin antibody. In the neonate, all the antibodies reacted with the junctional complex of podocytes in the S-shaped body stage. The staining disappeared during the capillary loop stage, when foot processes and slit diaphragms are formed. In the adult, podocytes were not stained with any of the antibodies, whereas distinct staining with the antibodies was detected in endothelial cells and mesangial cells in the glomerulus. These findings were identical in kidneys of PAN nephrosis; podocytes did not show any significant staining. These results indicate that the composition of intercellular junction molecules of podocytes in the adult is different from that of immature podocytes even under the pathological condition.

Coxsackievirus and Adenovirus Receptor, a Tight Junction Membrane Protein, Is Expressed in Glomerular Podocytes in the Kidney

“…These findings do not rule out the possibility that the junctional complex contains other types of junctions, such as adherens junction, because it has been shown in many cell lines that the formation of the epithelial junctional complex requires adherens junction proteins including cadherins and catenins (Gumbiner et al, 1988;Meyer et al, 1992). However, the newly formed junctions with close contact in PAN nephrosis did not react with any antibodies against cadherins or catenins (Usui et al, 2003;Yaoita et al, 2002a). CAR is unlikely to be associated with gap junctions because of different distribution of CAR compared with connexin43 in cultured podocytes.…”

Novel expression of claudin-5 in glomerular podocytes

“…It has been reported ultrastructurally that intercellular junctions of podocytes consist in slit diaphragms, tight junctions and gap junctions but not adherens junctions (Caulfield et al 1976;Pricam et al 1975;Rodewald and Karnovsky 1974). However, it remains controversial whether components of adherens junctions are contained in slit diaphragms (Reiser et al 2000;Usui et al 2003;Yaoita et al 2002a). Slit diaphragms are unique to podocytes and predominant under physiological conditions.…”

Activation of Canonical Wnt Signaling Meets with Podocytopathy

“…Some argue that given the known association between greater V and improved survival, normalizing urea removal to V (i.e., placing V in the denominator of Kt/V) seems illogical and may lead to suboptimal dialysis delivery to patients with small body habitus. 10 Others argue, in an era where high-efficiency dialyzers enable rapid removal of low molecular weight compounds, use of any urea-based metric of hemodialysis dose may result in treatment durations that are too short to enable adequate removal of middle molecules and excess volume. 4,11 Assuming that residual confounding did not overly influence results, the authors' demonstration that Kt/V urea is significantly associated with mortality offers a small modicum of support for the currently pervasive Kt/V urea -centric paradigm of hemodialysis dose titration.…”

“…9 A connection between canonical Wnt signaling and glomerulopathy has, until now, been far more tenuous, although the ␤-catenin complex is expressed at the slit diaphragm. 10 In addition, activation of integrin-linked kinase occurs in hereditary nephropathy, and unpublished observations in human podocytes identified nuclear translocation of ␤-catenin together with upregulation of glycogen synthase kinase 3␤ in association with specific NPHS1 mutations (A.K. and M. Saleem).…”