Figure 6
Figure 6. Effects of HIF1α deficiency on normal HSCs. (A) RT-PCR analysis for the expression of HIF1α, VEGF, GLUT1, TGFα, and PGK1 in WT or HIF1α−/− normal LSK cells and BCR-ABL–expressing LSK cells. (B) Gene set enrichment analysis of DNA microarray data displays gene expression profiling of HIF1α targets in WT or HIF1α−/− normal LSK cells and BCR-ABL–expressing LSK cells. (C) FACS analysis of HSCs in BM cells from WT or HIF1α−/− mice. The percentages of LSK cells (Lin−Sca-1+c-Kit+), LT-HSCs (Lin−Sca-1+c-Kit+CD34−CD135−), and ST-HSCs (Lin−Sca-1+c-Kit+CD34−CD135+) were similar in WT and HIF1α−/− mice; however, HIF1α−/− mice showed a higher percentage of MPP (Lin−Sca-1+c-Kit+CD34+CD135+) (n = 5). (D) Similar percentages of CD41−CD48−CD150+ Lin−Sca-1+c-Kit+ cells in BM cells of WT or HIF1α−/− mice (n = 3).

Effects of HIF1α deficiency on normal HSCs. (A) RT-PCR analysis for the expression of HIF1α, VEGF, GLUT1, TGFα, and PGK1 in WT or HIF1α−/− normal LSK cells and BCR-ABL–expressing LSK cells. (B) Gene set enrichment analysis of DNA microarray data displays gene expression profiling of HIF1α targets in WT or HIF1α−/− normal LSK cells and BCR-ABL–expressing LSK cells. (C) FACS analysis of HSCs in BM cells from WT or HIF1α−/− mice. The percentages of LSK cells (LinSca-1+c-Kit+), LT-HSCs (LinSca-1+c-Kit+CD34CD135), and ST-HSCs (LinSca-1+c-Kit+CD34CD135+) were similar in WT and HIF1α−/− mice; however, HIF1α−/− mice showed a higher percentage of MPP (LinSca-1+c-Kit+CD34+CD135+) (n = 5). (D) Similar percentages of CD41CD48CD150+ LinSca-1+c-Kit+ cells in BM cells of WT or HIF1α−/− mice (n = 3).

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