Does beta1-integrin-ligand disengagement induce in vitro capillary tube disruption mediated by p38 MAPK activity?
The beta1-integrin-ligand disengagement resulted in capillary disruption and stimulated p38 MAPK and ERK activity. In spite of activation of both pathways, the p38 MAPK but not the ERK pathway inhibitor prevented beta1-integrin antibody effects. Inhibiting p38 MAPK may mitigate capillary injury associated with sepsis and transplant rejection.
Continued expansion of excluded AAA sacs can occur from causes other than a missed endoleak. Exudation of fluid from thickened sac wall and vasa vasorum, as well as local enzymatic activity, might lead to the formation of a sac hygroma. Furthermore, these findings raise questions as to the need for surgical exploration of all patients with an enlarging AAA sac in the setting of low sac pressures and no definable endoleak.