Additional file 1: Table S1. of 2-amino-1-methyl-6-phenylimidazo(4,5-b) pyridine (PhIP) induces gene expression changes in JAK/STAT and MAPK pathways related to inflammation, diabetes and cancer

Global gene expression changes in h-MSC-derived adipocytes exposed to PhIP. (DOCX 24 kb

Phenotypic consequences of <i>OLR1 overexpression or inhibition</i>.

<p><b>A.</b> Wound healing assay. Upper panel - representative images of wound healing assay performed using HCC1143 cells transfected with either empty plasmid or <i>OLR1</i> cDNA vector; Lower panel – graph depicting the distance between edges of the wound after 36 hours of incubation. (*) – p<0.01; <b>B.</b> Adhesion assay. Upper panel- representative images of adherent non-transfected HCC1143 cells loaded with CellTracker Red CMTX (Invitrogen, Carlbad, CA) and applied to non-activated or activated (50 µg/ml oxLDL, 4 hrs) confluent HUVECs transfected with OLR1 Silencer or scrambled siRNA. Lower panel - graph depicting the number of adherent cells averaged from multiple fields of view in triplicate cultures. (*) – p<0.05 compared to non-activated control (“scrRNA”); (†) - p<0.05 compared to scrambled RNA; <b>C.</b> Colorimetric transendothelial migration assay. Upper panel – verification of the confluence of HUVECs on the membranes by staining cells with CellTracker Red CMTX. Lower panel – absorbance values of stain extracted from the cells migrated through TNFα-activated endothelial monolayer in presence of <i>OLR1</i> neutralizing antibody or human IgG (Control).</p

A list of transformation related genes influenced by <i>Olr1</i> deletion in mice.

<p>A list of transformation related genes influenced by <i>Olr1</i> deletion in mice.</p

<i>Olr1</i> deletion results in broad inhibition of NF-κB target genes.

<p>A diagram depicting a set of overlapping genes between transformation and <i>Olr1</i> KO transcriptomes. From the set of 238 genes upregulated during transformation, 26 genes were found to be inhibited in <i>Olr1</i> KO mice. Vast majority of these genes carried NF-κB sites in their proximal promoter sequences. In total, 86 NF-κB target genes were found to be inhibited in <i>Olr1</i> KO mice with enrichment for regulation of apoptosis (p = 0.0002), proliferation (p = 0.00003), wound healing (p = 0.0002), defense response (p = 0.0011), immune response (p = 0.0003) and cell migration (p = 0.0009).</p

NF-κB target genes outside of transformation pool significantly inhibited in Olr1 knockout mice (more than 1.2-fold).

<p>Legend: (^a)- a list of NFkB target genes was compiled from the following web-based databases: 1 - <a href="http://bioinfo.lifl.fr/NF-KB/" target="_blank">http://bioinfo.lifl.fr/NF-KB/</a>; 2 -<a href="http://people.bu.edu/gilmore/nf-kb/target/index.html#cyto" target="_blank">http://people.bu.edu/gilmore/nf-kb/target/index.html#cyto</a>; and 3 - <a href="http://www.broadinstitute.org/mpr/publications/projects/Lymphoma/FF_NFKB_suppl_revised.pdf" target="_blank">http://www.broadinstitute.org/mpr/publications/projects/Lymphoma/FF_NFKB_suppl_revised.pdf</a>. The genes whose expression was significantly altered by OLR1 deletion was analyzed for enrichment themes using DAVID bioinformatic database. The enriched themes included regulation of apoptosis, “A”; Wound healing,“W”; Cell proliferation, “P”; Defense response,“D”; Cell migration, “M”.</p