Figure 3. H. pylori stimulates proliferation in a PPARδ-dependent manner. (A).

MKN28 cells were transfected with control vector or dominant-negative (dn) PPARδ constructs, seeded in a three-dimensional culture system, and then infected with strain 7.13, or treated with the PPARδ agonist GW501516. Representative images are shown. (B) Following infection with strain 7.13, GW501516 or medium alone, cells were removed from Matrigel at 24-hour intervals and enumerated using Trypan blue staining. Error bars = SEM for experiments performed on at least 3 occasions. *p < .05 7.13-infected or GW501516-treated samples versus uninfected control. (C) MKN28 cells transfected with scrambled or PPARδ-specific siRNA were co-cultured with strain 7.13 for 48 hours. Total protein was analyzed by Western blot using an anti-PPARδ antibody. Bar graph represents densitometric analysis of multiple experiments. Error bars, SEM for all panels. *p < .05 versus uninfected scrambled control. #p < .05 versus 7.13-infected scrambled controls. (D) MKN28 cells transfected with scrambled or PPARδ-specific siRNA were seeded in Matrigel and infected with strain 7.13 or medium alone for 72 hours. BrdU was added to culture medium and ELISA for BrdU incorporation was performed. Error bars = SEM for experiments performed on at least 3 occasions. *p < .05 versus uninfected scrambled control. #p < .03 vs 7.13-infected scrambled control.