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. 2008 Dec 5;105(50):20009–20014. doi: 10.1073/pnas.0805171105

Fig. 3.

Fig. 3.

(A) DP receptor localized in tumor-vascular endothelial cells. Sections were double-labeled for DP receptor (green) and vascular endothelium (PECAM-1, red), and counterstained with DAPI (blue; n = 5). (Scale bar, 20 μm.) (B–D) DP deficiency accelerated, and daily DP agonism suppressed fibrinogen deposition and angiogenesis in tumors. Excised tumors were subjected to double immunostaining for PECAM-1 (green) and fibrinogen (red), and then counterstained with DAPI (blue). (Scale bar, 50 μm in B.) To quantify the angiogenic areas in the tumors, PECAM-1 staining was quantified relative to total pixel density (C). Fibrinogen deposition was normalized to total PECAM-1-positive pixel density (D; n = 6 each). (E) DP deficiency and DP agonism on tumor permeability. Mice bearing LLC tumors (on day 10 after the LLC implantation) were treated with vehicle (10 min), BW245C (50 μg/kg; i.v., 10 min). Tumors were excised and the Evans blue dye content was quantified (n = 6–8; *, P < 0.05 vs. WT and †, P < 0.05 vs. vehicle treatment).