Matrix metalloproteinase 2 genotype is associated with nonanastomotic biliary strictures after orthotopic liver transplantation

Hove, W. Rogier ten; Korkmaz, Kerem Sebib; Dries, Sanna op den; Rooij, Bert-Jan F. de; Hoek, Bart van; Porte, Robert J.; Reijden, Johan J. van der; Coenraad, Minneke J.; Dubbeld, Jeroen; Hommes, Daniël W.; Verspaget, Hein W.

doi:10.1111/j.1478-3231.2011.02459.x

Cited by 18 publications

(23 citation statements)

References 44 publications

(61 reference statements)

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“…Subsequent ischemic injuries caused by endothelial lesions increase the susceptibility to immunologic injury of biliary cells leading to ITBLs [62, 67, 145]. Preexisting primary sclerosing cholangitis and autoimmune hepatitis are also associated with a higher incidence of ITBLs [75, 76, 146]. …”

Section: Immunologically Mediated Itbls Following Ltmentioning

confidence: 99%

“…The SP C/T transition at position—1306 in the promoter of MMP-2, abolishes the single polymorphism 1 binding site and leads to decreased mRNA transcription and protein expression of MMP-2 [169, 170]. After LT, in association with the–1306 CT genotype of donor and recipient, the serum levels of MMP-2 were decreased in patients that developed ITBLs [75]. …”

Section: Immunologically Mediated Itbls Following Ltmentioning

confidence: 99%

“…MMP-2 CT genotype in both, donor and recipient is strongly and independently related to the development of ITBLs within 4 years after LT [75]. The presence of the MMP-2 CT genotype in donor and/or recipient was found to increase the incidence of ITBLs incidence stepwise from 9% when absent, increasing to 16% when present in either donor or recipient, further increasing to 29% when present in both donor and recipient [75].…”

Section: Immunologically Mediated Itbls Following Ltmentioning

confidence: 99%

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Ischemia-Reperfusion Injury and Ischemic-Type Biliary Lesions following Liver Transplantation

Cursio

Gugenheim

2012

Journal of Transplantation

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Ischemia-reperfusion (I-R) injury after liver transplantation (LT) induces intra- and/or extrahepatic nonanastomotic ischemic-type biliary lesions (ITBLs). Subsequent bile duct stricture is a significant cause of morbidity and even mortality in patients who underwent LT. Although the pathogenesis of ITBLs is multifactorial, there are three main interconnected mechanisms responsible for their formation: cold and warm I-R injury, injury induced by cytotoxic bile salts, and immunological-mediated injury. Cold and warm ischemic insult can induce direct injury to the cholangiocytes and/or damage to the arterioles of the peribiliary vascular plexus, which in turn leads to apoptosis and necrosis of the cholangiocytes. Liver grafts from suboptimal or extended-criteria donors are more susceptible to cold and warm I-R injury and develop more easily ITBLs than normal livers. This paper, focusing on liver I-R injury, reviews the risk factors and mechanisms leading to ITBLs following LT.

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Section: Immunologically Mediated Itbls Following Ltmentioning

confidence: 99%

Section: Immunologically Mediated Itbls Following Ltmentioning

confidence: 99%

Section: Immunologically Mediated Itbls Following Ltmentioning

confidence: 99%

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Ischemia-Reperfusion Injury and Ischemic-Type Biliary Lesions following Liver Transplantation

Cursio

Gugenheim

2012

Journal of Transplantation

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“…MMPs have been intensively studied and shown to play key roles in inflammation, carcinogenesis and regeneration and many researchers have already focused on MMP-2 and MMP-9 after liver surgery [12][13][14][15][16][17][18][19][20][21] . In the present study, 40% SOLT increased protein expression of MMP-2 in western blotting, although zymography did not show any differences.…”

Section: Survival Ratementioning

confidence: 99%

“…MMP-2 and MMP-9 are implicated in liver injury and remodeling. In particular, previous researchers reported that MMP-9 and MMP-2 contribute to liver failure after liver surgery [12][13][14][15][16][17][18][19][20][21] . Tissue inhibitors of metalloproteinases (TIMPs) are a family of endogenous inhibitors of MMPs.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress and extracellular matrices after hepatectomy and liver transplantation in rats

Hori¹,

Üemoto²,

Chen³

et al. 2014

WJH

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AIM:To investigate oxidative stress (OS)-mediated damage and the behavior of extracellular matrices in various rat models because shear stress with portal hypertension and cold ischemia/warm reperfusion injury trigger the liver regeneration cascade after surgery. These injuries also cause fatal liver damage. METHODS:Rats were divided into four groups according to the surgery performed: control; hepatectomy with 40% liver remnant (60% hepatectomy); orthotopic liver transplantation (OLT) with whole liver graft (100% OLT); and split OLT (SOLT) with 40% graft (40% SOLT). Survival was evaluated. Blood and liver samples were collected at 6 h after surgery. Biochemical and histopathological examinations were performed. OSinduced damage, 4-hydroxynonenal, ataxia-telangiectasia mutated kinase, histone H2AX, phosphatidylinositol 3-kinase (PI3K) and Akt were evaluated by western blotting. Behavior of extracellular matrices, matrix metalloproteinase (MMP)-9, MMP-2, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 were also evaluated by western blotting and zymography. RESULTS:Although 100% OLT survived, 60% hepatectomy and 40% SOLT showed poor survival. Histopathological, immunohistological, biochemical and protein assays revealed that 60% hepatectomy, 100% OLT and 40% SOLT showed liver damage. PI3K and Akt were decreased in 60% hepatectomy and 40% SOLT. For protein expression, 40% SOLT showed differences in MMP-9, MMP-2 and TIMP-2. TIMP-1 showed differences in 60% hepatectomy and 40% SOLT. For protein activity, MMP-9 demonstrated significant differences in 60% hepatectomy, 100% OLT and 40% SOLT. CONCLUSION: Under conditions with an insufficient liver remnant, prevention of OS-induced damage viathe Akt/PI3K pathway may be key to improve the postoperative course. MMP-9 may be also a therapeutic target after surgery. Hori T et al . Hepatic damage after liver surgeryCore tip: Although shear stress with portal hypertension and cold ischemia/warm reperfusion injury trigger the liver regeneration cascade after surgery, these injuries also cause fatal liver damage. Postoperative liver damage is still a critical matter in the field of liver surgery. Oxidative stress and extracellular matrices are important for liver regeneration after surgery and these may be important keys to overcome current problems in the field of liver surgery. Here, we investigated oxidative stress-mediated damage and the behavior of extracellular matrices in various rat models with liver surgery.Hori T, Uemoto S, Chen F, Gardner LB, Baine AMT, Hata T, Kogure T, Nguyen JH. ��idative stress and e�tracellular ma��idative stress and e�tracellular matrices after hepatectomy and liver transplantation in rats. World

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Meeting report of the 2011 joint international congress of the international liver transplantation society, the European liver and intestine transplant association, and the liver intensive care group of Europe

Levitsky

Guckelberger

2012

Liver Transpl

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The International Liver Transplantation Society held its yearly meeting as a joint conference with the European Liver and Intestine Transplant Association and the Liver Intensive Care Group of Europe at the Valencia Congress Center (Valencia, Spain) from June 22 to 25, 2011. Nearly 1500 registrants attended the meeting, which opened with a premeeting conference entitled “Global Challenges and Controversies in Liver Transplantation.” This was followed by numerous oral and poster abstract sessions and topic sessions focused on medical, surgical, and intensive care aspects of liver transplantation (LT). This report summarizes key symposia and oral abstracts delivered at the meeting and is conveniently divided into subsections relevant to LT. It is not meant to be a critical or comprehensive evaluation of all the meeting presentations and is merely intended to highlight presentations and associated published literature dealing with key topics. Liver Transpl 18:282–289, 2012. © 2011 AASLD.

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Matrix metalloproteinase 2 genotype is associated with nonanastomotic biliary strictures after orthotopic liver transplantation

Abstract: MMP-2 CT genotype of donor and recipient is an independent risk factor, in addition to PSC, for the development of NAS after OLT.

Cited by 18 publications

References 44 publications

Ischemia-Reperfusion Injury and Ischemic-Type Biliary Lesions following Liver Transplantation

Ischemia-Reperfusion Injury and Ischemic-Type Biliary Lesions following Liver Transplantation

Oxidative stress and extracellular matrices after hepatectomy and liver transplantation in rats

Meeting report of the 2011 joint international congress of the international liver transplantation society, the European liver and intestine transplant association, and the liver intensive care group of Europe

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