Fig. (13) Glomerular morphology (A-D), detection of glomerular podocalyxin (PODXL) abundance by immunohistochemistry (IHC, E-H), and electron-microscopic demonstration of anionic sites on the  surface of glomerular podocytes by polyethyleneimine (PEI) labeling (I-L) in a GH-transgenic mouse   (male, six week-old, NMRI background, B, F, J), a GIPR^dn-transgenic mouse (six-month-old, CD1   background, D, H, L), and associated age-matched control mice of the respective genetic background (A, E, I, and C, G, K). A-D: The GH-transgenic and the GIPR^dn-transgenic mouse display glomerular hypertrophy  and mesangial expansion and matrix accumulation (#). Additional lesions in the GH-transgenic mouse comprise  glomerular capillary hyalinosis, synechiae between the glomerular capillaries and the parietal epithelium of the  Bowman capsule (*), and tubular protein casts (open arrow in B). E-H: Compared to control mice (E, G), the  immunohistochemical PODXL staining intensity (brown color) at the surface of glomerular podocytes is reduced  in some glomeruli of the GH-transgenic mouse (F) and the GIPR^dn-transgenic mouse (H). Insets to F and G: IHC  negative controls. A-H: Paraffin sections, H & E staining (A-D). For IHC (E-H), DAB was used as chromogene  (brown color), and hemalaun as nuclear counterstain. Bars = 50 μm, and =10 μm in insets. E, F: Transmission  electron-microscopic (TEM) detection of anionic sites on podocyte surfaces with the cationic probe PEI. In non- transgenic control mice (I, K), the podocyte foot processes (fp) and the outer and inner laminae rarae of the  glomerular basement membrane (GBM) display regular, punctate, electron-dense labeling patterns (arrows). In  comparison, the broadened podocyte foot processes in some glomeruli of the GH-transgenic and the GIPR^dn-transgenic mouse show a slightly decreased number of PEI labeled anionic sites. Insets: Podocyte foot processes  of unlabeled control samples. Bars = 0.5 μm.