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>