Fig. 1
From: Complementary roles of KCa3.1 channels and β1-integrin during alveolar epithelial repair
Impact of KCa3.1 inhibition on fibronectin-stimulated ATII wound repair. ATII cell monolayers, grown in the absence (no coating) or presence of fibronectin coating, were injured mechanically and wound-healing rates were measured over a 24-h period, in the presence or absence of the KCa3.1 inhibitor TRAM-34. Representative photographs (x4 magnification) at time 0 (T0) and 24 h (T24) after injury in each condition are presented in (a). The wound edge is indicated by the dotted lines. b. Mean wound-closure rates (μm2/h) are compared in control (0) and TRAM-34 (5 and 10 μM) treated monolayers, in the absence or presence of fibronectin coating (n = 6). *p < 0.05