Inflammatory cytokine expression in healthy and CKD kidneys.

<p><b>A: Cytokine array in array.</b> Striped bars = 2K-CM (n = 6); dotted bars = 2K-NCM (n = 6); black bars = CKD-NCM (n = 7); white bars = CKD-CM (n = 4). IL-8 = interleukin 8; sICAM = soluble Inter-Cellular Adhesion Molecule; L-selectin = leucocyte cell-adhesion molecule; RANTES = Regulated upon Activation, Normal T-cell Expressed, and Secreted; MIG = Monokine Induced by Gamma-Interferon; MIP1α = Macrophage Inflammatory Protein-1 alpha; MIP3α = Macrophage Inflammatory Protein-3 alpha; Timp-1 = Tissue Inhibitor of Metalloproteinase 1; VEGF = Vascular Endothelial Growth Factor; IL-1RA = Interleukin 1 Receptor Antagonist. <b>B: Fractalkine mRNA in healthy and CKD kidneys.</b> Striped bars = 2K-CM (n = 6); dotted bars = 2K-NCM (n = 6); black bars = CKD-NCM (n = 7); white bars = CKD-CM (n = 4). *P<0.05: CKD vs. 2K.</p

Glomerulosclerosis was reduced by CM treatment.

<p>On PAS-stained sections, glomeurosclerosis was reduced after CM treatment (A). Normal (B), segmental (C) and totally sclerotic are shown (D). Black arrows indicate sclerotic areas. 2K-NCM (n = 6); 2K-CM (n = 6); CKD-NCM (n = 13); CKD-CM (n = 13). *P<0.05: CKD vs. 2K, †P<0.05: CKD-CM vs. CKD-NCM.</p

CM treatment increased DNA damage repair.

<p>After logarithmic transformation, more γ-H2AX positive cells, indicating glomerular nuclei undergoing DNA damage repair, were found after CM treatment in CKD (A). Black arrow indicates positive nucleus (B). 2K-NCM (n = 6); 2K-CM (n = 6); CKD-NCM (n = 13); CKD-CM (n = 13). *P<0.05: CKD vs. 2K.</p

Tubular collagen I and III deposition was reduced after CM treatment in CKD rats.

<p>CM treatment reduced sirius red staining (A). Raw (B) and polarized (C) pictures are shown. 2K-NCM (n = 6); 2K-CM (n = 6); CKD-NCM (n = 13); CKD-CM (n = 13). *P<0.05: CKD vs. 2K, †P<0.05: CKD-CM vs. CKD-NCM.</p

Tubulo-interstitial damage on PAS-stained sections was reduced after CM treatment in CKD rats.

<p>CM treatment decreased tubular fibrosis and atrophy (A). Differences between CKD (B) and healthy (C) tubular kidney tissue are shown. White arrow indicates infitration, black arrows showing proteincasts. 2K-NCM (n = 6); 2K-CM (n = 6); CKD-NCM (n = 13); CKD-CM (n = 13). *P<0.05: CKD vs. 2K, †P<0.05: CKD-CM vs. CKD-NCM.</p

CM stimulates in vitro angiogenesis (A) and wound closure (B).

<p>Average tube length was increased after CM treatment compared to NCM (C+D). In a scratch wound assay, CM treatment increased wound (indicated by black arrow in E) closure compared to NCM treatment. *P<0.05 CM vs. NCM.</p

Terminal kidney function measurements.

<p>Mean±SD *P<0.05: 2K vs. CKD.</p><p>MAP = mean arterial pressure. RBF = renal blood flow. RVR = renal vascular resistance. FF = filtration fraction. FeNa = fractional excretion of sodium. FeK = fractional excretion of potassium.</p

CM treatment increased the number of glomerular endothelial cells (A, C-D), but did not increase tubular endothelial cell number (B, E-F) shown by a JG12 staining.

<p>2K-NCM (n = 6); 2K-CM (n = 6); CKD-NCM (n = 13); CKD-CM (n = 13). *P<0.05: CKD vs. 2K, †P<0.05: CKD-CM vs. CKD-NCM.</p

Representation of experimental set up.

<p>UNX = uninephrectomy; SNX = subtotal nephrectomy; CM = conditioned medium administration. Stars indicate longitudinal measurements.</p

Longitudinal measurements after CM treatment at week 6 after SNX.

<p>Week numbers indicate the week after SNX. Week 5 represents the week before treatment.</p>*<p>P<0.05 vs. respective 2K controls. Posthoc p-value is shown.</p