Figure 6.

Transcription of p53 and major components of the ERK/MAPK pathway are regulated by nilotinib and the PDGFRα-D842V mutation. (A) PDGFRα⁺ iReFs were purified by magnetic beads from lungs of mice after 3 or 5 days of sham or PNX (white), PNX with nilotinib treatment (black), and PNX in PDGFRα-D842V mutants (gray). The RNA was extracted and complementary DNA prepared; then RT²-EGF/PDGF pathway arrays were performed in triplicates. Gene expression levels in the experimental groups were normalized to sham- and PNX-operated animals. PDGFRα⁺ iReFs were purified from lungs after 3 or 5 days of sham or PNX of wild-type, nilotinib-treated, or PDGFRα-D842V mutant mice. (B) Messenger RNA expression for PDGFRα, Ccnd2 (proliferation), acta2 (myo phenotype), Fabp4 (lipo phenotype). (C) Tenascin and periostin, (D) tropoelastin and clusterin, (E) vimentin and decorin, (F) Vinculin, Lox, Col23A, and osteonectin, and (G) FGFR4, IGFR1, Wnt2, and Wnt5a expressed in myo- and matrix-iRefs (n = 3–5). Data are expressed as mean ± SEM, and comparisons among groups were made by Student’s t test or analysis of variance, with P < 0.05 considered significant. IGFR, insulin growth factor receptor.