Microstructural changes of bile canaliculi in canine liver: the effect of cold ischemia–reperfusion in orthotopic liver transplantation

Yasui, Hitoshi; Yoshimura, Norio; Kobayashi, Yoshifumi; Ochiai, Seiji; Matsuda, Toshiki; Takamatsu, Tetsurou; Oka, Takahiro

doi:10.1016/s0041-1345(98)01222-6

Cited by 9 publications

(7 citation statements)

References 4 publications

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“…Actin cytoskeleton remodeling and hepatocyte BC integrity were reported as primary targets of IRI and have been shown to have direct functional implications on graft recovery in terms of bile secretion (5,10,11). However, the molecular mechanisms underlying these phenotypes remain incompletely characterized.…”

Section: Discussionmentioning

confidence: 99%

“…Treatment of rat liver with compounds that alter actin polymerization, such as cytochalasin B and phalloidin, leads to the alteration of BC structure (canaliculi dilatation and loss of microvilli) as well as contractile properties (8,9). In addition, a major actin cytoskeleton alteration around the hepatocyte cell membrane has been reported in human liver in response to IRI and has also been related to an impairment of BC contraction, tight junction permeability, and subsequent maintenance of a normal bile flow during the postoperative period (10,11). An intact actin network is therefore required for BC integrity to ensure proper bile secretion, i.e.…”

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confidence: 99%

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Proteomic Analysis of Ischemia-Reperfusion Injury upon Human Liver Transplantation Reveals the Protective Role of IQGAP1

Emadali

Muscatelli-Groux

Delom

et al. 2006

Molecular & Cellular Proteomics

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Ischemia-reperfusion injury (IRI) represents a major determinant of liver transplantation. IRI-induced graft dysfunction is related to biliary damage, partly due to a loss of bile canaliculi (BC) integrity associated with a dramatic remodeling of actin cytoskeleton. However, the molecular mechanisms associated with these events remain poorly characterized. Using liver biopsies collected during the early phases of organ procurement (ischemia) and transplantation (reperfusion), we characterized the global patterns of expression and phosphorylation of cytoskeletonrelated proteins during hepatic IRI. This targeted functional proteomic approach, which combined protein expression pattern profiling and phosphoprotein enrichment followed by mass spectrometry analysis, allowed us to identify IQGAP1, a Cdc42/Rac1 effector, as a potential regulator of actin cytoskeleton remodeling and maintenance of BC integrity. Cell fractionation and immunohistochemistry revealed that IQGAP1 expression and localization were affected upon IRI and related to actin reorganization. Furthermore using an IRI model in human hepatoma cells, we demonstrated that IQGAP1 silencing decreased the basal level of actin polymerization at BC periphery, reflecting a defect in BC structure coincident with reduced cellular resistance to IRI. In summary, this study uncovered new mechanistic insights into the global regulation of IRI-induced cytoskeleton remodeling and led to the identification of IQGAP1 as a regulator of BC structure.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Proteomic Analysis of Ischemia-Reperfusion Injury upon Human Liver Transplantation Reveals the Protective Role of IQGAP1

Emadali

Muscatelli-Groux

Delom

et al. 2006

Molecular & Cellular Proteomics

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“…Bile canalicular size change as detected in our study may be coincident with the reorganization of the pericanalicular filaments and the colocalization of actin and myosin. In fact, contraction in this study has been associated with shortening and/or twisting of canaliculi [5].…”

Section: Discussionmentioning

confidence: 50%

“…According to some authors, the use of the canine LT model seems to allow a better vascular perfusion under ex vivo conditions in contrast to the rat model [5]. All livers underwent perfusion with 5°C cold Ringer's solution into the portal and arterial system prior to cold ischemia at 5°C up to 10 h, related to hypothermia-induced change in hepatic metabolism similar to clinical LT, followed by a 2 h reperfusion period at 37°C.…”

Section: Discussionmentioning

confidence: 99%

Biliary-Type Cytokeratin Pattern in a Canine Isolated Perfused Liver Transplantation Model

Sergi

Groß

Mory

et al. 2008

Journal of Surgical Research

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“…1 In addition to injury to hepatocytes, this pathological process causes injury in the intrahepatic vascular and biliary systems seen as hepatic thrombosis or stenosis 2 and biliary strictures. 3,4 This leads to a high risk of liver dysfunctions and failure of liver transplantation. Regarding liver transplantation, the prevention of hepatic I/R injury has been a major research focus for therapeutic development owing to the scarcity of donated livers.…”

Section: Introductionmentioning

confidence: 99%

Ursodeoxycholyl lysophosphatidylethanolamide inhibits cholestasis- and hypoxia-induced apoptosis by upregulating antiapoptosis proteins

Sellinger

Pathil

et al. 2014

Exp Biol Med (Maywood)

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An increase of toxic bile acids such as glycochenodeoxycholic acid occurs during warm ischemia reperfusion causing cholestasis and damage in hepatocytes and intrahepatic biliary epithelial cells. We aim to test antiapoptosis effects of ursodeoxycholyl lysophosphatidylethanolamide under cholestatic induction by glycochenodeoxycholic acid treatment of mouse hepatocytes and hypoxia induction by cobalt chloride treatment of intrahepatic biliary epithelial cancer Mz-ChA-1cell line. Such treatments caused marked increases in apoptosis as evidenced by activation of caspase 3, caspase 8 and poly (ADP-ribose) polymerase-1. Co-treatment with ursodeoxycholyl lysophosphatidylethanolamide significantly inhibited these increases. Interestingly, ursodeoxycholyl lysophosphatidylethanolamide was able to increase expression of antiapoptotic cellular FLICE-inhibitory protein in both cell types. Ursodeoxycholyl lysophosphatidylethanolamide also prevented the decreases of myeloid cell leukemia sequence-1 protein in both experimental systems, and this protection was due to ursodeoxycholyl lysophosphatidylethanolamide's ability to inhibit ubiquitination-mediated degradation of myeloid cell leukemia sequence-1, and to increase the phosphorylation of GSK-3b. In addition, ursodeoxycholyl lysophosphatidylethanolamide was able to prevent the decreased expression of another antiapoptotic cellular inhibitor of apoptosis 2 in cobalt chloride-treated Mz-ChA-1 cells. Hence, ursodeoxycholyl lysophosphatidylethanolamide mediated cytoprotection against apoptosis during toxic bile-acid and ischemic stresses by a mechanism involving accumulation of cellular FLICE-inhibitory protein, myeloid cell leukemia sequence-1 and cellular inhibitor of apoptosis 2 proteins. Ursodeoxycholyl lysophosphatidylethanolamide may thus be used as an agent to prevent hepatic ischemia reperfusion.

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Microstructural changes of bile canaliculi in canine liver: the effect of cold ischemia–reperfusion in orthotopic liver transplantation

Cited by 9 publications

References 4 publications

Proteomic Analysis of Ischemia-Reperfusion Injury upon Human Liver Transplantation Reveals the Protective Role of IQGAP1

Proteomic Analysis of Ischemia-Reperfusion Injury upon Human Liver Transplantation Reveals the Protective Role of IQGAP1

Biliary-Type Cytokeratin Pattern in a Canine Isolated Perfused Liver Transplantation Model

Ursodeoxycholyl lysophosphatidylethanolamide inhibits cholestasis- and hypoxia-induced apoptosis by upregulating antiapoptosis proteins

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