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. 2013 Nov 19;1(6):e00163. doi: 10.1002/phy2.163

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© 2013 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society

Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

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Mechanisms and pathways responsible for reduction in Urografin-induced acute kidney injury. (A) Treatment of eNOS-deficient mice with Urografin caused a decrease in the kidney mRNA levels for the antiapoptotic proteins Bcl-2, APE1, and Ube2V1. Treatment of eNOS-deficient mice with PACAP reduced the Urografin-induced changes in the mRNA levels of all three antiapoptotic proteins, but the increase in the mRNA for Ube2V1 was not statistically significant. (B) Treatment of eNOS-deficient mice with Urografin caused an increase in the kidney mRNA levels of the nuclear receptor PPAR-α and the inducible enzyme HO-1. Treatment of eNOS-deficient mice with PACAP reduced the Urografin-induced change in the mRNA levels of PPAR-α but further increased the mRNA levels of HO-1. (C) Treatment of eNOS-deficient mice with Urografin caused an increase in the kidney mRNA levels of the innate immune system pattern recognition receptors TLR2, TLR4, and TLR6. Treatment of eNOS-deficient mice with PACAP reduced the Urografin-induced changes in the mRNA levels of all three pattern recognition receptors, but the decrease in the mRNA level for TLR4 was not statistically significant. (D) Treatment of eNOS-deficient mice with Urografin caused an increase in the kidney mRNA levels of the TLR adaptor proteins MyD88 and TRIF. Treatment of eNOS-deficient mice with PACAP reduced the Urografin-induced change in the mRNA levels for MyD88 and TRIF, but the decrease in the mRNA levels for TRIF was not statistically significant. *P < 0.05 and **P < 0.01 compared to the mice treated only with Urografin. Bars represent the mean ± SE. PACAP, pituitary adenylate cyclase-activating polypeptide; eNOS, endothelial nitric oxide synthase; TLR, Toll-like receptor; PPAR, peroxisome proliferator-activated receptor.