(A) H3K4m3 at the start of the TNF-α, MCP-1, and HO-1 genes. LPS-PC, maleate nephrotoxicity (Mal), and UUO each induced significant increases in the extent of H3K4m3 at exon 1 of the TNF-α and MCP-1 genes. Conversely, no change in H3K4m3 at HO-1 exon 1 was observed. CL, contralateral kidney in mice subjected to UUO. The CL results did not significantly differ from those observed in normal control (C) kidneys. (B) H3K4m3 at exons 4, 3, and 5 of the TNF-α, MCP-1, and HO-1 genes, respectively. H3K4m3 levels at both TNF-α and MCP-1 end exons were significantly increased with both UUO and LPS (but not maleate) preconditioning. Conversely, no increase in H3K4m3 was observed at HO-1 exon 5. Results in CL kidneys from UUO mice did not differ from normal controls (C).