Fig. 5.

Role of HIF-1α in CO-induced inhibition of apoptosis. (A) Mφs were exposed to a regimen of A/R to induce cell death (as described in Methods) in the presence of CO, conditioned media from cells exposed to CO for 24 h (CM), recombinant TGF-β, and a combination of CO plus neutralizing TGF-β (λTGF-β). Apoptosis was assessed by FACS analyses of propidium iodide. Results represent mean ± SD of four independent experiments. (B) A/R-induced apoptosis in mφs deficient in HIF-1α, Ad-CVL (BMDM from HIF-1α-Loxp mice + Ad-Cre), and vector control Ad-Y5 ± CO. Results represent mean ± SD from four independent experiments. (C) CO augments A/R-induced TGF-β expression, which is independent of IL-10. RAW 264.7 cells were pretreated with a neutralizing antibody to IL-10 (λIL-10) and then exposed to A/R ± CO as described above. Results are mean ± SD of four to six wells from three independent experiments ∗, P < 0.02 vs. Untx; ∗#, P < 0.001 vs. Air+A/R.