Figure 3.
Figure 3. Knockdown of HMGA2 impairs the in vivo reconstitution potential of CB-derived CD34+ cells. (A) Overview of the in vivo transplantation assay for HMGA2-deficient cells. (B) Human CD45+GFP+ chimerism in mice transplanted with shHMGA2-1–transduced cells as analyzed in peripheral blood after 7 and 14 weeks. (C) Representative FACS plots showing BM engraftment of primary recipient NSG mice 14 weeks after transplantation. (D) Accumulated data for huCD45+GFP+ cell engraftment, myeloid (CD15/CD33+), and lymphoid (CD19+) lineage distribution, as well as levels of HSC engraftment (CD34+CD38− cells) measured in huCD45+GFP+ graft in BM of primary recipient NSG. (E) Human CD45+GFP+ engraftment in secondary recipients analyzed 20 weeks posttransplantation. *P < .05; **P < .01.

Knockdown of HMGA2 impairs the in vivo reconstitution potential of CB-derived CD34+cells. (A) Overview of the in vivo transplantation assay for HMGA2-deficient cells. (B) Human CD45+GFP+ chimerism in mice transplanted with shHMGA2-1–transduced cells as analyzed in peripheral blood after 7 and 14 weeks. (C) Representative FACS plots showing BM engraftment of primary recipient NSG mice 14 weeks after transplantation. (D) Accumulated data for huCD45+GFP+ cell engraftment, myeloid (CD15/CD33+), and lymphoid (CD19+) lineage distribution, as well as levels of HSC engraftment (CD34+CD38 cells) measured in huCD45+GFP+ graft in BM of primary recipient NSG. (E) Human CD45+GFP+ engraftment in secondary recipients analyzed 20 weeks posttransplantation. *P < .05; **P < .01.

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