10.1371/journal.pone.0097985.g005 Jin Ma Jin Ma Steven J. Chadban Steven J. Chadban Cathy Y. Zhao Cathy Y. Zhao Xiaochen Chen Xiaochen Chen Tony Kwan Tony Kwan Usha Panchapakesan Usha Panchapakesan Carol A. Pollock Carol A. Pollock Huiling Wu Huiling Wu TLR4 deficiency protected diabetic kidneys from interstitial fibrosis and tubular injury. Public Library of Science 2014 cell biology Signal transduction cell signaling Membrane receptor signaling Immune receptor signaling Immunological signaling Molecular cell biology Metabolic disorders Diabetes mellitus Type 1 diabetes type 2 diabetes Nephrology Chronic kidney disease Model organisms Animal models Mouse models deficiency protected diabetic kidneys interstitial fibrosis tubular 2014-05-19 03:23:24 Figure https://plos.figshare.com/articles/figure/_TLR4_deficiency_protected_diabetic_kidneys_from_interstitial_fibrosis_and_tubular_injury_/1031190 <p>(A) Significant interstitial collagen accumulation was evident in WT but not TLR4<sup>−/−</sup> mice with diabetes at 12 and 24 weeks. (B) Illustration of representative sections of the histological changes on PSR staining for collagen. (C) Immunohistochemical staining showed upregulation of α-SMA in WT, but not TLR4<sup>−/−</sup> mice, with diabetes as compared to non-diabetic controls at week 24. (D) Significant upregulation of KIM-1 was apparent in WT mice with diabetes, but attenuated in TLR4<sup>−/−</sup> diabetic kidneys. The data are present as the means ± SEM; * <i>p</i><0.05; ** <i>p</i><0.01; *** <i>p</i><0.001. The number of animals per group was described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097985#pone-0097985-g001" target="_blank">Figure 1</a>.</p>