1. Renal denervation prevents long-term sequelae of ischemic renal injury
Jinu Kim, Babu J. Padanilam 
Kidney International 
Volume 87, Issue 2, Pages (February 2015)
DOI: /ki
Copyright © 2015 International Society of Nephrology Terms and Conditions

2. Figure 1
Renal denervation inhibits collagen deposition, and neutrophil and macrophage influx during a period of interstitial fibrosis after ischemia reperfusion injury (IRI). Two days after denervation in left kidneys of mice, IRI or sham operation (S) in the left kidneys was carried out. (a) Collagen deposition using Sirius red stain on denervated or intact kidney sections at 16 days after IRI. Bar=50μm. (b) Percentage of Sirius red-positive area on kidney sections. (c, d) Neutrophil infiltration represented by the number of polymorphonuclear neutrophil (PMN)-positive cells on immunohistochemically stained kidney sections. (c, e) Macrophage infiltration represented by the percentage of F4/80-positive area on immunohistochemically stained kidney sections. Error bars represent s.d. (n=5). #P<0.05 versus intact. Bar=50μm.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

3. Figure 2
Exogenous norepinephrine or calcitonin gene-related peptide enhances interstitial fibrosis and inflammation induced by ischemia reperfusion injury (IRI) in denervated kidneys. (a–c) Two days after denervation in left kidneys of mice, IRI or sham operation (S) in the left kidneys was carried out. (a) Kidney expression of tyrosine hydroxylase using western blot analysis at 16 days after IRI or sham. Anti-β-actin antibody served as a loading control. (b) Levels of norepinephrine and calcitonin gene-related peptide (CGRP) in the kidneys using enzyme-linked immunosorbent assay kits. (c) Immunohistochemical staining for CGRP on the kidney sections at 2 days after IRI. Bars = 50μm. (d–f) Denervation in left kidneys of mice was carried out; 2 days after the onset, norepinephrine, CGRP, or vehicle was continuously infused into the denervated kidneys via mini-osmotic pump, and the kidneys were subjected to 30min of ischemia followed by 16 days of reperfusion. (d) Percentage of Sirius red-positive area in kidneys sections. (e) Neutrophil infiltration represented by the number of polymorphonuclear neutrophil (PMN)-positive cells on immunohistochemically stained kidney sections. (f) Macrophage infiltration represented by percentage of F4/80-positive area on immunohistochemically stained kidney sections. Error bars represent s.d. (n=4). *P<0.05 versus sham, #P<0.05 versus intact, and $P<0.05 versus vehicle.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

4. Figure 3
α2-adrenergic receptor (AR) antagonist and calcitonin gene-related peptide (CGRP) receptor antagonist diminish interstitial fibrosis and inflammation induced by ischemia reperfusion injury (IRI). (a–c) Mice were continuously treated with doxazosin (α1-AR antagonist, 12mg/kg/day), atipamezole (α2-AR antagonist, 2.4mg/kg/day), pronethalol (β-AR antagonist, 2.4mg/kg/day), or 10% dimethyl sulfoxide (DMSO) in phosphate-buffered saline (PBS; vehicle) via an intraperitoneal implantation of mini-osmotic pump immediately before 30min of left kidney ischemia and 16 days of reperfusion. (a) Percentage of Sirius red-positive area on the kidney sections. (b) Neutrophil infiltration represented by counting polymorphonuclear neutrophil (PMN)-positive cells on immunohistochemically stained kidney sections. (c) Macrophage infiltration represented by percentage of F4/80-positive area on immunohistochemically stained kidney sections. (d–f) Mice were continuously treated with the CGRP receptor antagonist (CGRP(8-37), 120μg/kg/day) or 0.9% saline (vehicle) via an intraperitoneal implantation of mini-osmotic pump immediately before 30min of left kidney ischemia and 16 days of reperfusion. (d) Percentage of Sirius red-positive area on the kidney sections. (e) Neutrophil infiltration represented by the number of PMN-positive cells on immunohistochemically stained kidney sections. (f) Macrophage infiltration represented by percentage of F4/80-positive area on immunohistochemically stained kidney sections. Error bars represent s.d. (n=5). $P<0.05 versus vehicle.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

5. Figure 4
Norepinephrine and calcitonin gene-related peptide (CGRP) signaling contribute to kidney injury during a period of interstitial fibrosis after ischemia reperfusion injury (IRI). (a, d) Two days after denervation in left kidneys of mice, IRI or sham in the left kidneys was carried out (n=5). (c, e, f) Denervation or intact in left kidneys of mice was carried out; 2 days after the denervation, norepinephrine, CGRP, or vehicle was continuously infused into the denervated kidneys via mini-osmotic pump, and the kidneys were subjected to 30min of ischemia followed by 16 days of reperfusion (n=4). (a) Tubular damage represented by periodic acid–Schiff (PAS) stain on the kidney sections at 16 days after IRI. Bars=50μm. (b, c) Tubular injury score measured on PAS-stained kidney sections. (d, e) Glomerular filtration rate (GFR, creatinine clearance) was measured in mice housed in metabolic cages. (f) Kidney weight obtained from mice at 16 days after IRI or sham. Error bars represent s.d. #P<0.05 versus intact and $P<0.05 versus vehicle.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

6. Figure 5
Renal denervation reduces oxidative stress in a norepinephrine and calcitonin gene-related peptide (CGRP)-dependent manner in kidneys after ischemia reperfusion injury (IRI). (a) Two days after denervation in left kidneys of mice, IRI or sham in the left kidneys was carried out; then the kidneys were collected at 16 days after reperfusion (n=5). (b) Denervation in left kidneys of mice was carried out; 2 days after the onset, norepinephrine, CGRP, or vehicle was continuously infused into the denervated kidneys via mini-osmotic pump, and the kidneys were subjected to 30min of ischemia followed by 16 days of reperfusion (n=4). (a, b) Lipid peroxidation represented by level of lipid hydroperoxide in kidneys. Error bars represent s.d. #P<0.05 versus intact and $P<0.05 versus vehicle.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions

7. Figure 6
Renal denervation inhibits tubular cell cycle arrest in a norepinephrine and calcitonin gene-related peptide (CGRP)-dependent manner in kidneys after ischemia reperfusion injury (IRI). (a, b) Two days after denervation in left kidneys of mice, IRI or sham in the left kidneys was carried out (n=5). (c) Two days after denervation in left kidneys of mice, norepinephrine, CGRP, or vehicle was continuously infused into the denervated kidneys via mini-osmotic pump and the kidneys were subjected to 30min of ischemia followed by 16 days of reperfusion (n=4). (a) Immunohistochemial staining for phosphorylated histone H3 (p-H3) on kidney sections. Bars=50μm. (b, c) The number of p-H3-positive tubular cells on immunohistochemically stained kidney sections. Error bars represent s.d. #P<0.05 versus intact and $P<0.05 versus vehicle.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions