Kyrou Ioanna E, Papakostas John C, Ioachim Elli, Skoufi Urania, Koulouras Vasilios, Arnaoutoglou Eleni, Angelidis Charalampos, Matsagkas Miltiadis I
Department of Surgery-Vascular Surgery Unit, School of Medicine, University of Ioannina, and Department of Pathology, Hadjikosta General Hospital, Ioannina, Greece.
Ann Vasc Surg. 2013 May;27(4):480-6. doi: 10.1016/j.avsg.2012.08.009. Epub 2013 Mar 26.
Paraplegia after thoracoabdominal aortic surgery is a devastating complication attributed to motor neurons loss and dysfunction, due to spinal cord ischemia. β-Catenin is a protein that has been associated with cell survival and healing and many studies have correlated this protein with late ischemic preconditioning (IPC). Herein we investigate the potential contribution of β-catenin in an early IPC animal model, and its relationship with heat shock protein 70 (Hsp70), suggesting a possible role of this protein as a first window of protection.
A total of 42 pigs were used in an experimental thoracoabdominal aortic occlusion model. Twelve animals were used for neurologic evaluation and were randomly assigned to 2 groups (A and B). The remaining 30 animals were used in experiments for biologic measurements and innunohistochemical studies, and were randomly assigned to 5 groups (1-5). Western blotting analysis and immunoprecipitations were performed to study the levels of β-catenin and its binding relationship with Hsp70. The cellular distribution of β-catenin at various time-points was investigated by immunohistochemical studies.
According to neurologic evaluation, the animals in the IPC+ischemia group had significantly better neurologic scores compared with those in the ischemia group, indicating a protective role for IPC. The biologic measurements demonstrated a significant (P=0.03) increase in β-catenin levels and translocation of the protein in the nucleus at the end of ischemic preconditioning.
Our results suggest a significant role of β-catenin in early IPC protection of spinal cord after thoracoabdominal occlusion, as IPC seems to trigger the activation of the β-catenin stabilized fraction and, thus, its survival pathway.
