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. 2016 Apr 20;18(4):242–252. doi: 10.1016/j.neo.2016.03.001

Figure 6.

Figure 6

HIF-1α contributes to low MOI of H. pylori-induced Lonp1 induction and gastric cell proliferation. (A) Heatmap showing differential expression of known HIF-1α targets in Kx1 and Kx2 H. pylori infection models. (B-C) HIF-1α protein levels indicated by western blot (B) and HIF1a mRNA levels indicated by qPCR (C) in MKN28 gastric cells in response to low multiplicity of H. pylori infection at different time points (MOI = 50, NCTC 11637). (D) Hk2 and Pfkfb3, two HIF-1α targets, in MKN28 cells were transcriptionally elevated by low multiplicity of H. pylori infection (MOI = 50, NCTC 11637) for 12 hours. (E-F) Lonp1 protein levels (E) and mRNA levels (F) in HIF-1α-overexpressing MKN 28 cells (left) or HIF-1α-knockdown MKN28 cells in response to low multiplicity of H. pylori infection for 12 hours (MOI = 50, NCTC 11637) (right). (G) Cell growth of control and HIF-1α-overexpressing MKN28 gastric cells (left) or HIF-1α-knockdown cells in response to low multiplicity of H. pylori infection (right). Data represent the mean ± SEM from three separate experiments. * P < .05.