Skip to main content
. Author manuscript; available in PMC: 2009 Dec 28.
Published in final edited form as: Free Radic Biol Med. 2005 Apr 9;39(3):355–364. doi: 10.1016/j.freeradbiomed.2005.03.026

Fig. 7.

Fig. 7

HNE-mediated increase in AP-1 binding is via the ERK and p38 pathways. Cells were pretreated for 30 min with and without PD98059 (50 µM) and SB202190 (25 µM) to inhibit the ERK and p38 pathways, respectively. Data are expressed as a percentage of control AP-1 binding, with the control being arbitrarily set at 100%. The different experimental treatment groups were repeated at least four times and a representative EMSA is shown. HNE caused a significant increase in AP-1 binding that was blocked by both SB and PD.