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. 2006 Sep 15;36(2):138–146. doi: 10.1165/rcmb.2006-0253SM

Figure 1.

Figure 1.

Airway epithelial cell migration and wound repair is enhanced by NO. (A) Confluent NHBE and HBE1 cells (panels a and d) were wounded using a p-200 pipet tip and either untreated (panels b and e) or treated with DETA NONOate (10 μM) for 24 h (panels c and f). Confluent HBE1-NOS2 cells (panel g) were similarly injured and wound closure was monitored in the absence (panel h) or presence of the NOS inhibitor, l-NMMA, added 30 min before wounding (panel i). (B) Analysis of % wound closure using NIH ImageJ software to quantitate wound areas. (C) Analysis of % wound closure in NHBE (solid bars) and HBE1 (open bars) cells using varying doses of DETA NONOate (10–500 μM). (D) Cell migration was examined using 0.8-μm pore-size polycarbonate transwell membranes. NHBE1 (solid bars) and HBE1 (open bars) cells were either treated with l-NMMA or DETA NONOate (10 μM) and HBE1-NOS2 cells (shaded bars) were treated with l-NMMA where values are compared with HBE1 CTL. Data represent mean ± SE from at least three separate experiments.