Risk factor for ischemic-type biliary lesion after ABO-incompatible living donor liver transplantation

Bang, Jun Bae; Kim, Bong-Wan; Kim, Young Bae; Wang, Hee-Jung; Lee, Hyun Yeong; Sim, Joohyun; Kim, Taegyu; Lee, Kyeong Lok; Hu, Xuguang; Mao, Wei

doi:10.3748/wjg.v22.i30.6925

Cited by 12 publications

(6 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It may lead to intra- and extra-hepatic biliary stricture, bile duct injury and late graft loss, and is one of the reasons for retransplantation. [ 14 , 15 ] Several risk factors are discussed to be major parameters for the development of ITBL. Among them, prolonged ischemic times, reperfusion injury, disturbance in blood flow through the peribiliary vascular plexus, immunologically induced injury, cytotoxic injury, and ischemia reperfusion injury appear to have the most important influence.…”

Section: Discussionmentioning

confidence: 99%

Effect of HSP27 and Cofilin in the injury of hypoxia/reoxygenation on hepatocyte membrane F-actin microfilaments

Zhang

Wang²,

Ji³

et al. 2017

Medicine

View full text Add to dashboard Cite

Hypoxia–reoxygenation (H/R) injury hepatocyte models were established to simulate the ischemia/reperfusion injury of transplanted organ. Through the study of the molecular mechanism of H/R on the F-actin damage of the liver cytomembrane, the mechanism of F-actin damage induced by ischemia and reperfusion was studied from the level of cell and molecule.The hypoxic environment of cells in vitro was simulated by chemical hypoxia agent CoCl2. Liver cells were detected by MTT, H/R group was subdivided into 3 subgroups: H/R 2, 4, and 6 h. Changes of cell shape and the growth state, apoptosis, ultrastructural changes, and the changes in F-actin microfilament content were observed. Heat shock protein 27 (HSP27), Cofilin, and F-actin gene and protein levels were determined by real-time polymerase chain reaction and western blot assay, respectively.Cells showed circular adherence growth under normal circumstances, while the spindle cells and shedding cells were significantly increased in H/R groups. Apoptosis cells in H/R group were increased significantly with the extension of hypoxia time. The number of endoplasmic reticulum was decreased significantly in the H/R group, the mitochondrion hydropic was degenerated and the glycogen was disappeared. The F-actin fibers in the H/R group were disordered, the morphology of the fibers was obviously decreased, and the fluorescence staining decreased obviously (P < .05). The transcription and expression levels of HSP27, Cofilin, and F-actin were significantly lower than those in the control group (P < .05).These results demonstrate that H/R can affect the correct assembly of F-actin microfilaments and weakens the normal cycle of F-actin microfilaments through inhibiting the protein expression and gene transcription of HSP27 and Cofilin in hepatocytes, thereby changing the skeleton of F-actin microfilaments.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of HSP27 and Cofilin in the injury of hypoxia/reoxygenation on hepatocyte membrane F-actin microfilaments

Zhang

Wang²,

Ji³

et al. 2017

Medicine

View full text Add to dashboard Cite

show abstract

“…It has been reported that a large number of NK cells in recipient peripheral blood was the only risk factor for the induction of ischemic biliary tract disease after ABO-incompatible adult living donor liver transplantation. This may be explained that recipient NK cells could recognize various NK cell ligands on the donor endothelial cells after flowing into the liver graft, and the ABO antigen was abundantly expressed on the endothelial cells of the transplant graft, thereby directly producing cytotoxicity and resulting in decreased graft survival ( 48 , 49 ). Besides, there is a clinical study suggesting that recipient-derived NK cells are reduced but retain the robust expression of NK cell receptors such as NKG2D in the early stage of pediatric liver transplantation, which may be closely related to the increase of acute graft rejection episode ( 50 ).…”

Section: Function Of Nk Cells In Hepatic I/rmentioning

confidence: 99%

Natural Killer Cells in Hepatic Ischemia-Reperfusion Injury

et al. 2022

View full text Add to dashboard Cite

Ischemia-reperfusion injury can be divided into two phases, including insufficient supply of oxygen and nutrients in the first stage and then organ injury caused by immune inflammation after blood flow recovery. Hepatic ischemia-reperfusion is an important cause of liver injury post-surgery, consisting of partial hepatectomy and liver transplantation, and a central driver of graft dysfunction, which greatly leads to complications and mortality after liver transplantation. Natural killer (NK) cells are the lymphocyte population mainly involved in innate immune response in the human liver. In addition to their well-known role in anti-virus and anti-tumor defense, NK cells are also considered to regulate the pathogenesis of liver ischemia-reperfusion injury under the support of more and more evidence recently. The infiltration of NK cells into the liver exacerbates the hepatic ischemia-reperfusion injury, which could be significantly alleviated after depletion of NK cells. Interestingly, NK cells may contribute to both liver graft rejection and tolerance according to their origins. In this article, we discussed the development of liver NK cells, their role in ischemia-reperfusion injury, and strategies of inhibiting NK cell activation in order to provide potential possibilities for translation application in future clinical practice.

show abstract

“…ABOi deceased donor liver transplants are associated with a greater incidence of diffuse biliary strictures and in some series, inferior allograft survival, among adult recipients, but not young children . Several published series provide evidence of success among ABOi LDLT when there is modification of the preoperative and perioperative immunosuppression regimen with attention to isoagglutinin titers, but with an associated increased incidence of biliary complications . Furthermore, ABOi LDLT may not be ideal in certain clinical scenarios, particularly if the recipient has acute‐on‐chronic liver disease .…”

Section: Potential Indications For Lpementioning

confidence: 99%

“…(21)(22)(23) Several published series provide evidence of success among ABOi LDLT when there is modification of the preoperative and perioperative immunosuppression regimen with attention to isoagglutinin titers, but with an associated increased incidence of biliary complications. (21,(24)(25)(26) Furthermore, ABOi LDLT may not be ideal in certain clinical scenarios, particularly if the recipient has acute-on-chronic liver disease. (3) Except for young children, ABOi LDLT has not been performed in the United States, although 14 A2 donors have been used in non-A recipients (according to Organ Procurement and Transplantation Network/ UNOS data as of June 3, 2017).…”

Section: Abo Incompatibilitymentioning

confidence: 99%

Liver paired exchange: Can the liver emulate the kidney?

Mishra

Lee

et al. 2018

Liver Transpl

View full text Add to dashboard Cite

Kidney paired exchange (KPE) constitutes 12% of all living donor kidney transplantations (LDKTs) in the United States. The success of KPE programs has prompted many in the liver transplant community to consider the possibility of liver paired exchange (LPE). Though the idea seems promising, the application has been limited to a handful of centers in Asia. In this article, we consider the indications, logistical issues, and ethics for establishing a LPE program in the United States with reference to the principles and advances developed from experience with KPE. Liver Transplantation 24 677-686 2018 AASLD.

show abstract

Risk factor for ischemic-type biliary lesion after ABO-incompatible living donor liver transplantation

Abstract: High NK cell counts in a transplant recipient's blood are associated with ITBL after ABO-I ALDLT. Further research is needed to elucidate the molecular mechanism of NK cell involvement in the development of ITBL.

Cited by 12 publications

References 27 publications

Effect of HSP27 and Cofilin in the injury of hypoxia/reoxygenation on hepatocyte membrane F-actin microfilaments

Effect of HSP27 and Cofilin in the injury of hypoxia/reoxygenation on hepatocyte membrane F-actin microfilaments

Natural Killer Cells in Hepatic Ischemia-Reperfusion Injury

Liver paired exchange: Can the liver emulate the kidney?

Contact Info

Product

Resources

About