Figure_5.tif (1.95 MB)
TLR4 deficiency protected diabetic kidneys from interstitial fibrosis and tubular injury.
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posted on 2014-05-19, 03:23 authored by Jin Ma, Steven J. Chadban, Cathy Y. Zhao, Xiaochen Chen, Tony Kwan, Usha Panchapakesan, Carol A. Pollock, Huiling Wu(A) Significant interstitial collagen accumulation was evident in WT but not TLR4−/− 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−/− 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−/− diabetic kidneys. The data are present as the means ± SEM; * p<0.05; ** p<0.01; *** p<0.001. The number of animals per group was described in Figure 1.
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cell biologySignal transductioncell signalingMembrane receptor signalingImmune receptor signalingImmunological signalingMolecular cell biologyMetabolic disordersDiabetes mellitusType 1 diabetestype 2 diabetesNephrologyChronic kidney diseaseModel organismsAnimal modelsMouse modelsdeficiencyprotecteddiabetickidneysinterstitialfibrosistubular
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