Figure 4
Role of S1P in HIF-1α mRNA induction. (A) RAW264.7 cells were treated with the supernatant of apoptotic Jurkat cells (CMAC-J) for 16 hours in the presence or absence of 1 μM VPC23019 or 100 nM JTE-013. VPC23019 and JTE-013 were preincubated for 1 hour. (B) RAW264.7 cells were treated with the supernatant of apoptotic MCF-7 cells (CMAC-MCF7) or the supernatant of apoptotic MCF-7 cells with a knockdown of SK2 (CMAC-SK2kd), with or without the further addition of 500 nM S1P or 1 μM SEW2871 for 16 hours. HIF-1α as well as ribosomal 16S protein mRNA were determined by qRT-PCR. The ratio of HIF-1α versus ribosomal 16S protein mRNA under control conditions was set to 1. Data are the mean ± SD (n ≥ 3). *Significant alterations compared with controls (or otherwise as indicated).

Role of S1P in HIF-1α mRNA induction. (A) RAW264.7 cells were treated with the supernatant of apoptotic Jurkat cells (CMAC-J) for 16 hours in the presence or absence of 1 μM VPC23019 or 100 nM JTE-013. VPC23019 and JTE-013 were preincubated for 1 hour. (B) RAW264.7 cells were treated with the supernatant of apoptotic MCF-7 cells (CMAC-MCF7) or the supernatant of apoptotic MCF-7 cells with a knockdown of SK2 (CMAC-SK2kd), with or without the further addition of 500 nM S1P or 1 μM SEW2871 for 16 hours. HIF-1α as well as ribosomal 16S protein mRNA were determined by qRT-PCR. The ratio of HIF-1α versus ribosomal 16S protein 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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