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Journal of Diabetes Research
Volume 2016 (2016), Article ID 5362506, 11 pages
Research Article

Renal Protection by Genetic Deletion of the Atypical Chemokine Receptor ACKR2 in Diabetic OVE Mice

1Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA
2Department of Pathology, University of Louisville, Louisville, KY 40202, USA
3Department of Medicine, University of Louisville, Louisville, KY 40202, USA
4Department of Microbiology and Immunology, University of Louisville, Louisville, KY 40202, USA

Received 25 June 2015; Revised 25 September 2015; Accepted 27 September 2015

Academic Editor: Carlos Martinez Salgado

Copyright © 2016 Shirong Zheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplement Tables 1 and 2 show the 50 transcripts most reduced (Table 1) and most increased (Table 2) in OVE-ACKR2 kidney compared to OVE kidney. Only OVE-ACKR2 transcripts that were significantly different from OVE p≤0.05 are included. Values are the average signal ±SEM from a sample size of 3.

Supplement Figure 1 images show that most ACKR2 positive cells in diabetic human kidneys are tubule epithelial cells. In the upper panel ACKR2 staining is red and the proximal tubule brush border is labeled green with Lotus tetragonolobus lectin, a marker for kidney tubule brush border. The lower panel is a DIC image showing that the central tubule has an almost continuous brush border adjacent to nearly continuous ACKR2 stained cells. In both images most ACKR2 staining is on tubule epithelial cells with a brush border.

  1. Supplementary Material