Figure 7
Figure 7. Distinct GR isoforms in human DCs. Human monocyte–derived DCs were cultured as described in “Methods.” (A) A representative Western blot analysis shows that the GR isoform switched from the GR-D (predominantly GR-D1) to the GR-A isoform after LPS (1 ng/mL, 24 hours) treatment. The ratio (± SD, n = 3) of the proapoptotic GR-A isoform over the nonapoptotic GR-D isoforms (GR-A/D) increased significantly by LPS (1 ng/mL, 24 hours; 2-tailed t test, *P < .01). (B) Representative histograms show the distinct sensitivity of control (CON) and LPS-treated cells to DEX (100nM, 48 hours). Cell death was indicated by the amount of DAPI staining. The average results (± SD, n = 4) are also shown (*significantly greater than other treatment groups, P < .05; 1-way ANOVA followed by Tukey posthoc test).

Distinct GR isoforms in human DCs. Human monocyte–derived DCs were cultured as described in “Methods.” (A) A representative Western blot analysis shows that the GR isoform switched from the GR-D (predominantly GR-D1) to the GR-A isoform after LPS (1 ng/mL, 24 hours) treatment. The ratio (± SD, n = 3) of the proapoptotic GR-A isoform over the nonapoptotic GR-D isoforms (GR-A/D) increased significantly by LPS (1 ng/mL, 24 hours; 2-tailed t test, *P < .01). (B) Representative histograms show the distinct sensitivity of control (CON) and LPS-treated cells to DEX (100nM, 48 hours). Cell death was indicated by the amount of DAPI staining. The average results (± SD, n = 4) are also shown (*significantly greater than other treatment groups, P < .05; 1-way ANOVA followed by Tukey posthoc test).

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