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AND AIMS: Endothelial dysfunction is crucial in the pathophysiology of LPS-induced AKI. Endothelial cells (EC) acquired a fibroblast-like phenotype and contributed to myofibroblasts generation through EndMT process.. Noteworthy, ARPCs enhance tubular regenerative mechanism during AKI, but little is known about their effects on EC. The aim of this study was to understand whether ARPCs could preventsepsis-induced EndMT and to identify the related mechanisms. METHODS: EC were stimulated in vitro with LPS (4lg/ml) for 48h, co-cultured with ARPCs for 24h, and analyzed by MTT assay and FACS. Gene expression profile was obtained from ARPCs and LPS-stimulated ARPCs by Agilent SurePrint G3 Human Gene Expression Microarrays. Genespring and R software were used for the analysis. Gene expression was validated by Real-time PCR and ELISA. AKI was induced by i.v. LPS infusion (300ug/kg) in swine model. Renal biopsies, were performed before and at 9h from LPS infusion , and were analyzed by IF.

nephrology, dialysis, transplantation/nephrology dialysis transplantation

FP211A CLUSTER OF PROTEINS SECRETED BY HUMAN RENAL STEM/PROGENITOR CELLS (ARPCS) PROVIDE A NOVEL STRATEGY TO REVERT ENDOTHELIAL DYSFUNCTION AND RENAL INJURY IN SEPSIS-INDUCED ACUTE KIDNEY INJURY (AKI)