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. Author manuscript; available in PMC: 2010 Oct 13.
Published in final edited form as: Cell Commun Insights. 2009;2:1–11. doi: 10.4137/cci.s2775

Figure 5.

Figure 5

PAI-1 induction in TGF-β1-stimulated tubulogenic cells requires EGFR signaling. Pretreatment with the EGFR inhibitor AG1478 or the MMP/ADAM inhibitor GM6001 effectively attenuated both ERK1/2 phosphorylation and PAI-1 induction in TGF-β1-stimulated T2 cells; addition of both AG1478 and GM6001 simultaneously completely ablated both responses. (A) EGFR signaling was similarly required for PAI-1 expression in TGF-β1-treated HMEC-1 cultures. (B, C) While PAI-1 induction was effectively blocked by prior incubation with AG1478, SMAD2 phosphorylation was retained indicating that TGF-βR signaling was not impacted by this pharmacologic inhibitor. (C) The combination of AG1478 and GM6001 pretreatment was particularly effective at ablating ERK1/2 phosphorylation and PAI-1 in response to either singular (A–C) or dual (D) growth factor stimulation.