Table 1. LAP-induced monocyte chemotaxis is blocked by specific inhibitors of LAP-TSP-1 interactions.
| Inhibitor Treatment of Monocytes | Fold-change in monocyte recruitment to LAP vs. “Untreated” control | P value |
| Untreated | 4.3±1.0 | |
| Anti-LAP IgG | 1.3±0.4 | <0.05 |
| Anti-TGF-β1 IgG | 4.3±0.7 | ns |
| anti-TSP-1 IgG | 1.1±0.1 | <0.01 |
| anti-CD36 IgG | 1.2±0.1 | <0.001 |
| anti-CD47 IgG | 6.2±0.7 | ns |
| Isogenic Control Antibody | 3.0±0.5 | ns |
| LSKL | 0.9±0.2 | <0.01 |
| SLLK | 3.3±0.5 | ns |
| RGD-blocking peptide | 6.5±0.6 | ns |
| Scramble RGD-blocking peptide | 8.2±2.4 | ns |
| UO126 MEK inhibitor | 1.2±0.3 | <0.01 |
Human monocytes (5×104/condition) were suspended in Gey's balanced salt solution and assayed for their chemotactic response to rhLAP. Recruitment was assayed by incubating monocytes in modified Boyden chambers for 90 minutes at 37°C and quantified by counting five high-powered fields of stained membranes in a blinded fashion and reported as fold-increase of LAP (10 pg/ml)-induced monocyte chemotaxis compared to monocyte chemotaxis induced by media alone. rhLAP at 10 pg/ml was chosen based on previous experiments that determined this dose induced maximal cellular recruitment. These data represent n = 3 (minimum) separate experiments expressed as the mean fold-change±SEM. Reported p values compare fold-change in monocyte chemotaxis induced by LAP without and with identified inhibitors.