Allograft Inflammatory Factor-1 Induction during Ischemia Reperfusion Injury: A Rat Model of LAD Occlusion

The emerging role of the innate immune response in organ transplantation heightens the significance of molecular markers released from the donor organ due to ischemia/reperfusion injury (IRI) during organ procurement. These molecules are prime activators of innate immunity. Allograft inflammatory factor-1 (AIF1) has been implicated in the regulation of inflammation and organ rejection. To verify expression level of AIF-1 in cardiac tissues, we developed a rat model of IRI, in which the left anterior descending artery (LAD) was occluded to generate ischemia in the left ventricle (LV) of the heart. Blood and cardiac tissues were tested for the presence of AIF-1 at different time intervals. AIF-1 expression was significantly increased in a time-dependent manner after IRI. AIF1 was up regulated as early as 10 minutes after reperfusion, and further it was increased several-fold after 60 minutes of reperfusion in PBMCs and PMNCs as compared to the control group. Expression levels of AIF-1 in LV tissues were significantly increased after 60 minutes of ischemia or 30 minutes of ischemia followed by 60 minutes of reperfusion. In addition the level of AIF-1 was 2-fold greater in LV tissues after 60 minutes of reperfusion compared to LV after 30 or 60 minutes of ischemia, Thus, myocardial IRI activates AIF-1 up-regulation, which may result in allograft dysfunction in transplantation settings.