Katrien Vandoorne1, Tegest Aychek2, Hagit Dafni1, Brian A. Hemmings3, Steffen Jung2, Michal Neeman1
1Biological Regulation, Weizmann Institute, Rehovot, Israel; 2Immunology, Weizmann Institute, Rehovot, Israel; 3Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland
The etiology of inflammatory bowel disease (IBD), a group of inflammatory conditions of the intestinal tract, remains largely unknown. Akt1, a protein kinase, is a major mediator of angiogenic signaling, acting downstream of vascular endothelial growth factor (VEGF). In this study, we reported significantly decreased permeability (PS) in Akt1 deficient mice using macromolecular DCE-MRI, validated by histology. This decreased permeability of albumine-based contrast agent implies less leakage of plasma proteins and thus, limited disease progression. These results provide direct evidence that Akt1 enhances DSS-induced colitis. MRI proved to provide high sensitivity for in vivo detection of reduced permeability in colitis.