IMEX   05356
INSTITUTO DE MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Shiga toxin type 2, a causal agent of hemolytic uremic syndrome, improved angiogenic and repair abilities of late outgrowth endothelial progenitor cells
Autor/es:
LANDONI VI; SCHATTNER M; MENA HA; RODRIGUEZ RODRIGUES N; NEGROTTO S; SCHIERLOH P; FERNANDEZ, G
Lugar:
Berlin
Reunión:
Congreso; ISTH Congress; 2017
Institución organizadora:
ISTH
Resumen:
Hemolytic Uremic Syndrome (HUS), the main cause of pediatric acute renal failure, is caused by E. coli producing Shiga toxins (Stx) and characterized by massive endothelial damage, which is worsened by inflammation, especially in the presence of bacterial lipopolysaccharides (LPS). Endogenous regeneration of the vessel wall involves local and bone marrow-derived endothelial progenitor cells (EPC) as well as nearby mature endothelial cells (EC). Although Stx toxic effects on mature EC have been widely studied, its action on EPC and angiogenesis remain to be elucidated. We aimed to analyze the effect of Stx alone or in combination with LPS on survival and angiogenic properties of EPC.Human cord blood-derived late-outgrowth EPC and umbilical vein EC were cultured in endothelial growth medium EGM2. Cells were sensitized with LPS (500 ng/mL) for 18 h and then Stx type 2 (5-50 ng/mL) was added for another 18 h. Nuclear morphology analysis revealed that Stx, at concentrations that induce mature EC death, had no effect on EPC survival cultured in basic medium (EBM2+ 2% FBS), which undergo apoptosis only after LPS sensitization (Fig.1). Moreover, no Stx effect was observed when EPC were cultured on EGM2 (Fig.1). Stx receptor Gb3 was expressed on EPC surface and upregulated after LPS+Stx treatment (180±12*% of untreated control, n=3, *p