One possible reason for suppression of specific genes such as IL-1[beta] or CXCL2 and CXCL3 through the overexpression of AhRR is the interaction of AhRR with yet unidentified DNA sequences on the promoter regions of these particular genes.
The highest increase of more than 1,700-fold was found for CXCL5 followed by CXCL2 and CXCL3 in adipose.
These genes include MCP-1, IL-8, CXCL1, CXCL2,
CXCL3, and CXCR4.
Four (IL8, ILIA, PTGS2,
CXCL3) were related to inflammatory response, three (IL8, ILIA, DTR) related to regulation of cell proliferation, and two (DTR, TNFAIP3) related to gene transcription.
The ELR motif-positive CXC chemokines, CXCL1, CXCL2,
CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8, can directly promote the migration and proliferation of endothelial cells and eventually neovascularization [37] (Figure 4).
Angiogenic ELR+ Antiangiogenic chemokines non-[ELR.sup.+] chemokines CXCL1 CXCL4 CXCL2 CXCL9
CXCL3 CXCL10 CXCL5 CXCL11 CXCL6 CXCL14 CXCL7 CXCL8