FIGURE 1:

JAM-A regulates barrier function. (A) Treatment of SK-CO15 with σ1 (10 μg/ml) on plating abrogates the formation of TER compared to cells treated with mutant σ1_G381A (representative experiment with three independent samples; mean ± SD). (B) Treatment of confluent SK-CO15 monolayers with σ1 (20 μg/ml) for 1 h led to significant reduction in TER compared to cells treated with σ1_G381A mutant (representative experiment with three independent samples; mean ± SD). (C) Treatment of confluent SK-CO15 monolayers with σ1 (20 μg/ml) for 1 h led to significant reduction in JAM-A expression at tight junctions. (D) Administration of σ1 in vivo enhances permeability to small molecules. WT σ1 or σ1_G381A (100 μg/ml) was administered to intestinal loops of WT mice for 1 h and then assessed for 3-kDa dextran flux for another hour (n = 3 per group; mean ± SEM). For all experiments, *p < 0.05, **p < 0.01, ***p < 0.001 between groups at each time point per Student's t test.