Ligation of protease-activated receptor 1 enhances α_v β₆ integrin–dependent TGF-β activation and promotes acute lung injury
J. Clin. Invest. R. Gisli Jenkins, et al. 116:1606 doi:10.1172/JCI27183 [Go to this article.]

Figure 2
Stimulation of lung epithelial cells with a PAR1 agonist leads to α_v β₆ -dependent TGF-β activation. (A) IMLE cells were cocultured with TML cells and stimulated with increasing doses of SFLLRN, and luciferase activity from the TGF-β–responsive plasminogen activator inhibitor-1 promoter was measured. IMLE cells expressing human WT β₆ (black bars) were compared with IMLE cells that had no cell surface β₆ (white bars), and both were also stimulated with increasing doses of SFLLRN in the presence of α_vβ₆ blocking antibody (IMLE β₆-positive, dark gray bars; IMLE β₆-negative, light gray bars). (B) To determine the proportion of TGF-β expression that was mediated by α_vβ₆ in epithelial cell cultures, IMLE cells and normal human bronchial epithelial (NHBE) cells were stimulated with 10 μM of SFLLRN (gray bars), in the absence or presence of an α_vβ₆ blocking antibody (black bars) or a pan–TGF-β blocking antibody (white bars), in coculture with TML cells, and luciferase activity was measured. All experiments were performed in triplicate, and the mean + SEM is shown. Results are a representative example of at least 2 identical independent experiments.