Platelet activation and increased tissue factor expression on monocytes in reperfusion injury following orthotopic liver transplantation.
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Platelet activation and increased tissue factor expression on monocytes in reperfusion injury following orthotopic liver transplantation. / Esch, Jan Schulte Am; Jurk, Kerstin; Knoefel, Wolfram T; Roeder, Gesine; Voss, Holger; Tustas, Roy Y; Schmelzle, M; Krieg, Andreas; Eisenberger, Claus F; Topp, Stefan; Rogiers, Xavier; Fischer, Lutz; Aken, Hugo Van; Kehrel, Beate E.
In: PLATELETS, Vol. 21, No. 5, 5, 2010, p. 348-359.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Platelet activation and increased tissue factor expression on monocytes in reperfusion injury following orthotopic liver transplantation.
AU - Esch, Jan Schulte Am
AU - Jurk, Kerstin
AU - Knoefel, Wolfram T
AU - Roeder, Gesine
AU - Voss, Holger
AU - Tustas, Roy Y
AU - Schmelzle, M
AU - Krieg, Andreas
AU - Eisenberger, Claus F
AU - Topp, Stefan
AU - Rogiers, Xavier
AU - Fischer, Lutz
AU - Aken, Hugo Van
AU - Kehrel, Beate E
PY - 2010
Y1 - 2010
N2 - Platelets have been implicated in the pathogenesis of liver damage after orthotopic liver transplantation (OLT). Early graft dysfunction is frequently caused by reperfusion injury subsequent to cold ischemia (IRI). Therefore, we investigated activation of the pivotal haemostatic cells, platelets and monocytes, from patients with elevated markers of IRI and from patients with uneventful course (control-group), respectively during the first week after OLT. Flow cytometry analysis of citrate anticoagulated blood samples revealed that platelets from IRI patients became significantly activated within 48 h after OLT in vivo, with increased surface presentation of P-selectin, CD40L, thrombospondin-1 and tissue-factor. Platelet activation in IRI patients on post-transplant day 2 was accompanied by significantly enhanced tissue-factor expression on peripheral blood monocytes, significant elevated levels of C-reactive protein and hepatocellular damage. Towards post-transplant day 4, levels of platelet-derived microparticles rose significantly in IRI patients if contrasted to control patients. Thus, activated cellular haemostasis is involved in the early inflammatory response of hepatocellular damage subsequent to reperfusion of the transplanted liver. Targeting distinct activation patterns of platelets and monocytes in an early phase of hepatic grafting may counteract the extent of IRI via inhibition of micro-thrombus formation and inflammation without exacerbating the existing bleeding risk.
AB - Platelets have been implicated in the pathogenesis of liver damage after orthotopic liver transplantation (OLT). Early graft dysfunction is frequently caused by reperfusion injury subsequent to cold ischemia (IRI). Therefore, we investigated activation of the pivotal haemostatic cells, platelets and monocytes, from patients with elevated markers of IRI and from patients with uneventful course (control-group), respectively during the first week after OLT. Flow cytometry analysis of citrate anticoagulated blood samples revealed that platelets from IRI patients became significantly activated within 48 h after OLT in vivo, with increased surface presentation of P-selectin, CD40L, thrombospondin-1 and tissue-factor. Platelet activation in IRI patients on post-transplant day 2 was accompanied by significantly enhanced tissue-factor expression on peripheral blood monocytes, significant elevated levels of C-reactive protein and hepatocellular damage. Towards post-transplant day 4, levels of platelet-derived microparticles rose significantly in IRI patients if contrasted to control patients. Thus, activated cellular haemostasis is involved in the early inflammatory response of hepatocellular damage subsequent to reperfusion of the transplanted liver. Targeting distinct activation patterns of platelets and monocytes in an early phase of hepatic grafting may counteract the extent of IRI via inhibition of micro-thrombus formation and inflammation without exacerbating the existing bleeding risk.
KW - Adult
KW - Humans
KW - Male
KW - Female
KW - Middle Aged
KW - Prospective Studies
KW - Inflammation blood
KW - Case-Control Studies
KW - Blood Platelets physiology
KW - Liver blood supply
KW - Liver Diseases blood
KW - Liver Transplantation physiology
KW - Monocytes metabolism
KW - Platelet Activation physiology
KW - Reperfusion Injury blood
KW - Thromboplastin biosynthesis
KW - Adult
KW - Humans
KW - Male
KW - Female
KW - Middle Aged
KW - Prospective Studies
KW - Inflammation blood
KW - Case-Control Studies
KW - Blood Platelets physiology
KW - Liver blood supply
KW - Liver Diseases blood
KW - Liver Transplantation physiology
KW - Monocytes metabolism
KW - Platelet Activation physiology
KW - Reperfusion Injury blood
KW - Thromboplastin biosynthesis
M3 - SCORING: Zeitschriftenaufsatz
VL - 21
SP - 348
EP - 359
JO - PLATELETS
JF - PLATELETS
SN - 0953-7104
IS - 5
M1 - 5
ER -
