Imatinib mesylate inhibits the profibrogenic activity of TGF-β and prevents bleomycin-mediated lung fibrosis
J. Clin. Invest. Craig E. Daniels, et al. 114:1308 doi:10.1172/JCI19603 [Go to this article.]

Figure 2
TGF-β2 activation of c-Abl is independent of PDGFR signaling. (A) NIH-3T3 cells were treated for the indicated times with TGF-β2 (10 ng/ml) or PDGF-AB (25 ng/ml). Cell lysates were prepared and processed for c-Abl kinase activity (first panel), total c-Abl protein (second panel), tyrosine-phosphorylated PDGF-β receptor (p-PDGFR; third panel), or total PDGF-β receptor (fourth panel) as described in Methods. (B) NIH-3T3 cells were treated as described in Figure 1. PDGF-α and -β receptor–null F cells were seeded at 1.5 × 10⁶ cells per 100-mm dish. Following overnight growth, the medium was replaced with serum-free DMEM alone (PDGFR^–/–) or adenovirus (MOI 100) expressing the type I and type II TGF-β receptors (Ad.TGF-βRI and Ad.TGF-βRII, respectively) for 24 hours. Cultures were left untreated (–) or stimulated (+) with 10 ng/ml TGF-β2 for 30 minutes and processed for c-Abl kinase activity (first panel), or total c-Abl (second panel), PDGF-β receptor (third panel), type I TGF-β receptor (TGF-βRI; fourth panel), or type II TGF-β receptor (TGF-βRII; fifth panel) protein.