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. 2012 Aug 17;61(9):2280–2288. doi: 10.2337/db11-1138

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© 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 1. — Diabetes drives TrkA expression in affected kidneys. A: Five biopsy specimens of patients with DN (i) and tissues from human control individuals (ii) were stained with PAS; representative photomicrographs are shown. B: Immunohistochemistry for TrkA was performed in all biopsy specimens and representative microphotographs of DN and control tissue are shown. C: Real-time PCR for TrkA expression in specimens of tissues from kidneys of HC patients (n = 3) and DN patients (n = 4) was performed. Results are shown as fold change normalized to one of the HC samples. D: Phosphorylated form of TrkA (Y490) was detected with specific antibody in DN but was not present, or barely detectable, in control specimens (blue-purple, hematoxylin counterstain of nuclei; brown, specific stain of TrkA). E: A murine model of DN (DBA/2-Ins2^Akita, lower panel) and DBA/2 control (upper panel) mice were probed immunohistochemically for CD31 expression, a marker of endothelial cells (brown, CD31; blue-purple, hematoxylin nuclear counterstain) and for TrkA (brown, TrkA; blue-purple, hematoxylin nuclear counterstain). Data for n = 6 mice; representative photomicrographs are shown. The arrows indicate CD31-positive cells in glomeruli; arrowheads indicate TrkA staining in tubules. F: CD31-postive glomerular cells were counted in control mice and compared with CD-31 positivity in glomeruli of DN mice. The error bars in C and F show the SD. (A high-quality digital representation of this figure is available in the online issue.)