Figure 2
CM induces HIF-1 activity in RAW264.7 and primary mouse macrophages. (A) RAW264.7 cells were transfected with the pGL-3xEPO-HRE plasmid and treated with 100 μM CoCl2 or the supernatant of apoptotic Jurkat cells (CMAC-J) for 16 hours. Control conditions were set to 1. (B-C) RAW264.7 cells or (E-F) primary mouse macrophages were incubated under 1% hypoxia (H) or treated with CMAC-J for 16 hours. Glut-1 (B,E) and VEGF (C,F) as well as ribosomal 16S protein mRNA were determined by qRT-PCR. The ratio of ribosomal 16S protein versus Glut-1 or VEGF mRNA under control conditions was set to 1. Data are the mean ± SD (n ≥ 3). *Significant alterations compared with controls (or otherwise as indicated).

CM induces HIF-1 activity in RAW264.7 and primary mouse macrophages. (A) RAW264.7 cells were transfected with the pGL-3xEPO-HRE plasmid and treated with 100 μM CoCl2 or the supernatant of apoptotic Jurkat cells (CMAC-J) for 16 hours. Control conditions were set to 1. (B-C) RAW264.7 cells or (E-F) primary mouse macrophages were incubated under 1% hypoxia (H) or treated with CMAC-J for 16 hours. Glut-1 (B,E) and VEGF (C,F) as well as ribosomal 16S protein mRNA were determined by qRT-PCR. The ratio of ribosomal 16S protein versus Glut-1 or VEGF mRNA under control conditions was set to 1. Data are the mean ± SD (n ≥ 3). *Significant alterations compared with controls (or otherwise as indicated).

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