Additional Supporting Information may be found in the online version of this article.

STEM_1047_sm_SuppFig1.tif1586KFigure 1s. Schematic of the experimental protocol. RAS: renal artery stenosis, ARAS: atherosclerotic RAS, PTRA: percutaneous transluminal renal angioplasty, MSC: mesenchymal stem cells.
STEM_1047_sm_SuppFig2.pdf671KFigure 2s. A: Spindle-shaped MSC expanded from adipose tissue. B: Adipose MSC secreted VEGF and TNF-α in culture. Cultured MSC expressed mesenchymal markers (CD44, CD90, and CD105), but not endothelial (CD31) or inflammatory (CD14 and CD45) markers.
STEM_1047_sm_SuppFig3.pdf669KFigure 3s. Adipose MSC transdifferentiated into osteocytes (Ms xh Osteocalcin), chondrocytes (Gt xh Aggrecan), and adipocytes (Gt x msFABP-4) in vitro (A). Very few fluorescent CM-DiI (arrows, 40x) MSC were observed in the contralateral kidney (B) or myocardium (C) 4 weeks after intra-renal delivery.
STEM_1047_sm_SuppFig4.pdf640KFigure 4s. Top: Stenotic kidney renal tissue sections stained with proliferating cell nuclear antigen (PCNA) (left) and endothelial cell marker CD31 (right) 4 weeks after MSC administration. Single staining for CM-DiI (arrows, 40×) showing engrafted-MSC (middle) that co-stained with both PCNA and CD31 (bottom).
STEM_1047_sm_SuppFig5.pdf872KFigure 5s. Treatment with MSC increased the number of proliferating cell nuclear antigen (PCNA, green) positive cells (A) and the staining for the endothelial cell markers CD31 (green) and Von Willebrand factor (vWF, brown) 4 weeks after intra-renal delivery (B). *p<0.05 vs. normal, †p<0.05 vs. ARAS+PTRA+MSC.
STEM_1047_sm_SuppInfo.pdf61KSupplementary Data

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