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. 2016 Mar 4;23(7):1243–1256. doi: 10.1038/cdd.2016.19

Figure 7.

Figure 7

ANXA1 enhances IAV-induced apoptosis. Wild-type and Annexin-A1 (ANXA1)−/− deficient mice were infected intra-tracheally with influenza A/PR/8/34. Lungs were extracted at 3 days post-infection and apoptosis was assessed using (a) caspase 3 or 7 cleavage or (b) Annexin-V/PI staining. Tubulin was used as a loading control. (c and d) A549 lung epithelial cells (control or shRNA silenced for ANXA1 (ANXA1-sh) were infected with 1 MOI of influenza A/PR8. Cell viability was assessed after 24 h using crystal violet staining. (e) Caspase-3 activity was measured in control or ANXA1-siRNA A549 cells uninfected or infected with 1 MOI of influenza A/PR/8/34 for indicated times. *P<0.05; **P<0.01 versus 0. (f) A549 cells were infected with media (M) or indicated MOI of influenza A/PR8 for 24 h. Cell lysates were subjected to immunoblot analysis for the indicated antibodies. GADPH was used as a loading control. (g and h) Scramble and ANXA1-shRNA transfected A549 cells were infected with 1 MOI of influenza A/PR8 and cells were lysed at the indicated time points and subjected to immunoblot analysis for the indicated antibodies. (i) Scramble and ANXA1-shRNA transfected A549 cells were infected with 5 MOI of influenza A/PR8 and cells were fractionated into mitochondrial and cytosolic fractions at the indicated time points and subjected to immunoblot analysis for the indicated antibodies. AIF was used as a mitochondrial loading control and GAPDH was used as a cytosolic loading control