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Fig. 1 | Cardiovascular Diabetology

Fig. 1

From: Klotho inhibits renal ox-LDL deposition via IGF-1R/RAC1/OLR1 signaling to ameliorate podocyte injury in diabetic kidney disease

Fig. 1

Renal-specific deposition of ox-LDL was associated with podocyte injury in DKD. A Serum levels of ox-LDL were measured using an ELISA assay in healthy control (HC, n = 10) individuals and DKD patients at stage III (n = 10). B, C IF analysis using the podocyte nuclear marker WT1 and the membrane marker Nephrin revealed that some of the ox-LDL deposition was located along the surface of podocytes, as indicated by the presence of ox-LDL deposits in the glomeruli of DKD patients and mice, in comparison to HC and wild-type (WT) individuals. D Further confirmation was obtained through IF, demonstrating the deposition of ox-LDL along the podocyte membrane. This deposition occurred specifically between Integrin β1, a component of the glomerular basement membrane, and Nephrin, the marker protein of the podocytes. E IF staining was performed using the mesangial cell nuclear marker GATA3 and the membrane protein marker PDGFRβ to assess the presence of ox-LDL within mesangial cells in the glomeruli of DKD patients and mice. F Representative Western blot and summarized data showing the effects of ox-LDL on the relative protein levels of apoptosis-associated cleaved Caspase3 and podocyte marker, WT1 and Podocin, in HG-induced podocytes. G IF staining of podocytes exposed to high HG and ox-LDL reinforcing the strong connection between renal ox-LDL deposition and podocyte injury under HG conditions. For all statistical plots, the data are presented as the mean ± SD; ns no significant; *P < 0.05; **P < 0.01; ***P < 0.001

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