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Figure 2. Role of endothelial E-selectin in the control of HSC and LSC. (Left) under steady-state conditions, few bone marrow endothelial cells express the adhesion molecule E-selectin on their surface, mediating in few instances the interaction with the CD44 receptor expressed on HSCs; (middle) under conditions of bone marrow regeneration following damage caused by radiotherapy or chemotherapy, E-selectin expression on bone marrow endothelial cells markedly increases and promotes HSC proliferation; (right) in AML patients, the inflammatory microenvironment promotes a marked increase of E-selectin expression on bone marrow endothelial cells, mediating its interaction with the CD162 receptor overexpressed on the surface of LSCs. GMI-1271, a E-selectin inhibitor, blocks the interaction between E-selectin and CD162, reducing the binding of LSCs to endothelium and their chemoresistance. HSC: hematopoietic stem cell; LSC: leukemic stem cell