Figure 7.

MSCs adhesion to fibrin hydrogels and fibrinolysis effect. MSCs from the three tissues cultured in fibrin hydrogels exhibited elongated and round phenotypes, with actin in filaments or aggregates, respectively. Vinculin and integrin αV were not necessary for adhesion, as they were absent in FAs, and only some cells were positive for both proteins. Proportions of elongated and round-shaped cells varied between the three types of MSCs accordingly to their capabilities to degrade fibrin hydrogel. PL-MSCs were rounded in >90%, degraded the hydrogel completely, and generated a monolayer with FAs rich in vinculin (see Supplemental Figure S1), and were positive probably for integrin αV (as it was shown in 2D cultures, see Figure 5). BM-MSCs and WJ-MSCs degraded fibrin in a limited way, and after 3 days they still gathered inside it. In all cases, aprotinin and tranexamic inhibited fibrinolysis more than BB-94, meaning that it was done principally via the plasminogen–plasmin axis. uPA: urokinase plasminogen activator; tPA: tissue plasminogen activator; PAI-1: plasminogen activator inhibitor 1; MMPs: metalloproteases; TIMPs: tissue inhibitors of metalloproteases.