Polyclonal anti-thymocyte globulins influence apoptosis in reperfused tissues after ischaemia in a non-human primate model

Transplant International : Official Journal of the European Society for Organ Transplantation
Andres Beiras-FernandezClaus Hammer

Abstract

Reperfusion triggers the expression of inflammatory cytokines and adhesion molecules that increase the rate of apoptosis in the reperfused tissues after ischaemia, thus worsening the outcome of the grafts. Polyclonal anti-thymocyte globulins (pATGs) are able to reduce the number of lymphocytes as well as block adhesion molecules and induce apoptosis in T-lymphocytes through Fas-ligand. The aims of this study were to investigate the influence of pATGs on the prevention of apoptosis of reperfused tissues after ischaemia and to monitor their capability to enhance lymphocyte apoptosis thus decreasing the deleterious effects of ischaemia/reperfusion injury (IRI). Extremities of cynomolgus monkeys ( n=8) were flushed via either the femoral or the brachial artery. After 60 min of ischaemia the limbs were reperfused with human blood. ATG was added to the blood in a therapeutic dose 20 min prior to reperfusion of the extremities. Surgically available limbs ( n=20) were assigned to the following groups: ATG group ( n=10) and control group (without ATG; n=10). DNA fragmentation analysis was performed in situ to detect apoptosis at the single-cell level. Our study shows an increased rate of muscle and connective tissue apoptosis in the con...Continue Reading

References

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Citations

Sep 27, 2012·Journal of Inflammation·Jason S HawksworthDoug K Tadaki
Jul 11, 2006·Transplant International : Official Journal of the European Society for Organ Transplantation·Waichi WongNina Tolkoff-Rubin
Dec 17, 2014·Transplantation Proceedings·M RafieiJ Kobashigawa
Aug 30, 2016·Transplant International : Official Journal of the European Society for Organ Transplantation·Jamila KremerBruno K Podesser

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis