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. 2013 Mar;48(3):337–345. doi: 10.1165/rcmb.2012-0393OC

Figure 1.

Figure 1.

Nicotinamide adenine dinucleotide phosphate–reduced oxidase (NADPH) oxidase activation contributes to wound responses in murine tracheal epithelial (MTE) cells. (A) Confluent MTE cell monolayers on chamber slides were loaded with H2 DCF for 30 minutes before scratch wounding with a pipette tip in the absence (a and b) or presence of inhibitors of NADPH oxidase (diphenylene iodonium; 1 μM; c and d) or purinergic P2Y receptors (suramin, 100 μM; e and f). DCF fluorescence was measured 10 minutes after wounding. Ctl, control. (B) Wound closure after scratch injury of MTE cell monolayers was followed for 24 hours in the absence or presence of DPI (1 μM), the P2YR antagonists suramin (100 μM) or reactive blue–2 (RB-2; 100 μM), or the ATPase Apyrase (10 U/ml). CTL, control. Data represent the mean ± SE of four replicates from two separate experiments. *P < 0.05, compared with untreated control samples.