Shiga toxin type 2, a causal agent of hemolytic uremic syndrome, improved angiogenic and repair abilities of late outgrowth endothelial progenitor cells.

AGUSTINA MENA; LANDONI VERÓNICA INÈS; SHIERLOH P; NAHUEL RODRIGUEZ-RODRIGUES; SCHATTNER M; FERNÁNDEZ, GC; NEGROTTOS

Berlin

Congreso; International Society on Thrombosis and Haemostasis 2017 Congress and 63th Annual SSC Meeting; 2016

Hemolytic Uremic Syndrome (HUS), the main cause of pediatric acute renalfailure, is caused by E. coli producing Shiga toxins (Stx) and characterized bymassive endothelial damage, which is worsened by inflammation, especiallyin the presence of bacterial lipopolysaccharides (LPS). Endogenous regenerationof the vessel wall involves local and bone marrow-derived endothelialcolony forming cells (ECFC) as well as nearby mature endothelial cells (EC).Although Stx toxic effects on mature EC have been widely studied, its actionon ECFC and angiogenesis remain to be elucidated. We aimed to analyze theeffect of Stx alone or in combination with LPS on survival and angiogenic propertiesof ECFC.