Fig 1: Comparison of relative expressions of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 in the high risk, moderate risk, and low risk groups.
Fig 2: ICAM-1 secreted by colon cancer cells promotes survival under acidic microenvironment. (a) First row, HCT15 cells were cultured in pH 7.4 or pH 6.5 medium; second row, HCT15 cells were cultured in pH 6.5 medium with 1/3 pH 7.4 or pH 6.5 condition medium and measured with colony-forming assay after 12 d. (b) HCT15 cells were treated as in (a), and apoptosis was measured by flow cytometry. (c) Soluble ICAM-1 concentration was measured by ELISA. (d) Expression of ICAM-1 was determined by Western blotting. (e) Flow cytometric analysis of ICAM-1 levels in CRC-AA and their parental cells. (f) Knockdown of ICAM-1. HCT15 and HCT15-AA cells were transfected with siRNA for 48 h; RNAi efficiency was determined by Western blotting. GAPDH was used as a loading control. (g) HCT15 cells were cultured in pH 7.4 or pH 6.5 medium, with addition of CRC-AA conditioned medium, CRC-AA siICAM-1 conditioned medium, or ICAM-1 recombinant protein. The level of apoptosis was measured by flow cytometry. (h) DCF intensity in CRC and CRC-AA cells transfected with ICAM-1 siRNA for 24 h. (i) HCT15 cells were cultured in pH 7.4 or pH 6.5 medium, with addition of CRC-AA conditioned medium or ICAM-1 recombinant protein; ROS levels were measured by flow cytometry analysis of DCF. (j) NF-κB-dependent expression of ICAM-1. p65 was depleted by siRNA for 48 h in HCT15 and HCT15-AA cells. ICAM-1 and p65 protein levels were determined by Western blotting. (k) Schematic model showing the role of the GATA4-NF-κB pathway driven by autophagy in CRC-AA cells. ∗p < 0.05; ∗∗p < 0.01; ns, p > 0.05.
Fig 3: Correlation between ICAM-1 mRNA gene expression and serum ICAM-1 levels.
Fig 4: HDL suppresses Aß-induced monocyte adhesion in engineered vessels via SR-BI. SR-BI blocking antibody was circulated through the lumen of engineered vessels prepared using HUVEC for 1 h prior treatment with 200 µg/mL of HDL for 2 h followed by injection of 1 µM of monomeric a Aß40 or b Aß42 within the tissue chamber (abluminal) for 8 h prior to injecting circulating fluorescent THP1 into the lumen. c-d ICAM-1 protein was measured in tissue lysates prepared in RIPA buffer by commercial ELISA. Graphs represent means ± SD of adhered monocytes relative to Aß treated tissues from at least 4 individual grafts. * and # p < 0.05
Fig 5: PL inhibited TNF-α-induced expression of adhesion molecules and pro-inflammatory chemokines in HUVECs. (A–D) HUVECs were incubated under normal condition or TNF-α stimulation with or without PL. The mRNA expression levels of ICAM-1, VCAM-1, MMP-2 and MMP-9 were analyzed by qRT-PCR. Ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001. (E) The secretions of ICAM-1, VCAM-1, MMP-2 and MMP-9 in different groups were detected by ELISA. #, *P < 0.05, ###, ***P < 0.001. (# compares TNF-α 20 ng/ml conditions with normal condition and * compares PL 5 μM condition with 0.1% DMSO condition).
Supplier Page from Abcam for Human ICAM1 ELISA Kit (CD54)