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. 2014 Oct 16;9(10):e110388. doi: 10.1371/journal.pone.0110388

Figure 7. Deletion of TXNIP augments hyperoxia-induced ASK-1 activation and apoptotic markers.

Figure 7

Wild type (WT) and TXNIP knockout (TKO) mice were subjected to 5 days hyperoxia (p7–12). Retinas were collected for protein ASK-1 (A) and apoptotic markers (Cleaved Caspase-3 and PARP) (B). A 2×2 analysis showed a significant interaction between gene (TKO) and oxygen levels (Hyperoxia) in activation of ASK-1. In parallen, Hyperoxia caused significant increase in cleaved caspase-3 and PARP expression compared to normoxia in WT and TKO. Reduced Trx levels were associated with a significant increase in activation of the apoptotic ASK-1, PARP and caspase-3 pathway. (#P<0.05 Hyperoxia vs Normoxia, *P<0.05, TKO vs WT, n = 4–6).