Figure 1. FTVI- and FTVII-mediated α(1,3)-exofucosylation equally create sLe^X determinants on hMSCs derived from either bone marrow (BM-hMSCs) or adipose tissue (A-hMSCs).

(A): Representative flow cytometry histograms of HECA452 mAb (left) and E-Ig (right) staining of hMSCs that were untreated (black line) or treated either with FTVI (dotted line) or FTVII (dashed line). Grey filled histogram represents staining with isotype control. As assessed by HECA452 and E-Ig staining, both types of hMSCs natively lack sLe^X epitopes, each of which are uniformly created after FTVI or FTVII treatment. (B and C): Representative western blot analysis of whole cell lysates of untreated, FTVI- and FTVII-treated hMSCs resolved by SDS-PAGE and stained with HECA452 mAb (B) or anti-CD44 mAb (C). Lysates of KG1a cells serve as positive control for HECA452 blot results. Exofucosylation of both types of hMSCs prominently engenders a HECA452-reactive glycoprotein of mw ~90kDa (B) that has mobility profile equivalent to that of CD44 (C). For all figures, data are representative of five independent experiments. Abbreviations: FTVI, Fucosyltransferase VI; FTVII, Fucosyltransferase VII; BM-hMSCs, Bone Marrow-derived human Mesenchymal Stem Cells; A-hMSCs, Adipose-derived human Mesenchymal Stem Cells; E-Ig, E-selectin-immunoglobulin Fc chimera.