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. 2020 Dec 21;9(12):2723. doi: 10.3390/cells9122723

Figure 6.

Figure 6

NO and VE-cadherin are downstream of PAR1 in TEM-regulating endothelial signalling. (A) GPNT were pre-treated for 2 h and maintained with BAPTA (20 μM), compound C (CC, 10 μM), DEANO (50 μM) or SCH79797 (1 μM) and the indicated compound combinations. PAS were added and TEM was assessed 4 h. (B) GPNT were transfected with either pEGFP-N’-mVEC WT or Y731E encoding wild type mouse VE-cadherin or the phosphomimetic mutant Y731E and grown to confluency for 24–48 h. GPNTs were then either left untreated (mVEC WT, Y731E) or pre-treated with and maintained in PAR1 non-peptide antagonist SCH79797 (SCH, 1 µM) for 2 h. L-NAME pre-treatment (LN, 1 mM) was administered 1 h before PAS were added to the monolayer. Data represented as normalised means −/+ SEM. Each data point represents one independent, biological replicate. Significant differences were determined by ANOVA and Tukey’s post-hoc analysis (v control or pairwise as indicated). * p < 0.05, ** p < 0.01, *** p < 0.001. (C) Proposed signalling network downstream of PAR-1 and ICAM-1.