| Popis: |
Growth inhibitory effect of collagen via the activation of the p38 signal in A549-DDR2 S768R. (A) Cellular proliferation of transfectant A549 cell lines. Cellular growth was examined using an MTT assay with or without stimulation with collagen I (10 µg/mL). Without collagen I, the cellular proliferation of A549-DDR2 S768R was significantly enhanced, compared with the controls. In contrast, under exposure to collagen I, the cellular proliferation was particularly reduced, similar to that in the A549-DDR2 WT cell line. Furthermore, the proliferation of the A549-DDR2 E655K cell line was significantly enhanced, compared with that of A549-DDR2 S768R cell line, under exposure to collagen I. Columns, mean of independent triplicate experiments; Bars, SD; *, P < 0.05; n.s., not significant. (B) Western blotting of the MAPK signal pathways in the A549-S768R cell line. The phosphorylation of ERK1/2, c-Jun, or JNK were not enhanced after exposure to collagen I. In contrast, the phosphorylation of p38 in the A549-DDR2 S768R cell line was enhanced 6 or 24 hours after stimulation with collagen I. β-actin was used as an internal control. (C) Cellular proliferation of the A549-DDR2 S768R cell lines with or without exposure to a p38 inhibitor (SB202190, 1 µM) in the presence of collagen I (10 µg/mL). Cellular growth was examined using an MTT assay. When the A549-DDR2 S768R cell line was treated with SB202190, the suppression of proliferation by collagen stimulation was cancelled. Columns, mean of independent triplicate experiments; Bars, SD; *P < 0.05. |
