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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Proximal tubule-derived exosomes contribute to mesangial cell injury in diabetic nephropathy via miR-92a-1-5p transfer

Fig. 1

Identifying the presence of proximal tubular epithelial cell (PTEC)-derived exosomes which promoted myofibroblast transdifferentiation (MFT) in mesangial cells (MCs). A Transmission electron microscope (TEM) analysis revealed exosomes in the secretion of PTECs. B The surface markers of exosomes derived from HK-2 cells treated with normal glucose (NG, 5.5 mM) or high glucose (HG, 25 mM) using western blotting. C Detection of NG- or HG-treated HK-2 cell-derived exosomes uptake by mouse mesangial cells (MMCs) using immunofluorescence stain. D MFT markers were assessed in MMCs treated with condition medium of HK-2 cells under NG and HG conditions for 48 h using a co-culture system. E MFT markers were assessed in MMCs treated with exosomes derived from HK-2 cells under NG and HG conditions for 48 h (HK-2 cells: MMCs = 5:1). F, G The expression of N-cadherin and collagen I in kidneys of mice and humans. Kidney sections of non-diabetic db/m mice (n = 4) and diabetic db/db mice (n = 4) at 12th week, and human donors (upper tract urothelial carcinoma (UTUC)) with normal kidney function and normal glomeruli) (n = 4) and patients with DN (n = 4) were stained with N-cadherin and collagen I (brown) and α-smooth muscle actin (SMA, green). H MMCs were treated with condition medium (CM) derived from HK-2 cells under NG and HG conditions, HG-induced HK-2 cell CM after removing exosomes, and HG-induced HK-2 cell-derived exosomes for 48 h. Western blotting was used to measure N-cadherin, vimentin, collagen I and E-cadherin protein expression. The images quantification was performed using the IHC Profiler Plugin of ImageJ Software. The bar graph represents the mean ± S.E.M. of at least three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 by Student’s t-test or ANOVA followed by the post hoc test with Tukey’s correction

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