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Benkoël, L; Dodero, F; Hardwigsen, Jean; Campan, P.; Botta‐Fridlund, Danielle; Lagadic‐Gossmann, Dominique; Treut, Yves Patrice Le; Chamlian, A

doi:10.1023/a:1010693218680

Cited by 27 publications

(9 citation statements)

References 28 publications

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“…In contrast to CPF animals, cytoskeleton reorganization appears to be taking place wherein cytoskeletal genes are decreasing (Figure 3). This finding is concordant with previous reports of cytoskeleton destabilization following reperfusion [30].…”

Section: Resultssupporting

confidence: 94%

Fed State Prior to Hemorrhagic Shock and Polytrauma in a Porcine Model Results in Altered Liver Transcriptomic Response

et al. 2014

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Hemorrhagic shock is a leading cause of trauma-related mortality in both civilian and military settings. Resuscitation often results in reperfusion injury and survivors are susceptible to developing multiple organ failure (MOF). The impact of fed state on the overall response to shock and resuscitation has been explored in some murine models but few clinically relevant large animal models. We have previously used metabolomics to establish that the fed state results in a different metabolic response in the porcine liver following hemorrhagic shock and resuscitation. In this study, we used our clinically relevant model of hemorrhagic shock and polytrauma and the Illumina HiSeq platform to determine if the liver transcriptomic response is also altered with respect to fed state. Functional analysis of the response to shock and resuscitation confirmed several typical responses including carbohydrate metabolism, cytokine inflammation, decreased cholesterol synthesis, and apoptosis. Our findings also suggest that the fasting state, relative to a carbohydrate prefed state, displays decreased carbohydrate metabolism, increased cytoskeleton reorganization and decreased inflammation in response to hemorrhagic shock and reperfusion. Evidence suggests that this is a consequence of a shrunken, catabolic state of the liver cells which provides an anti-inflammatory condition that partially mitigates hepatocellar damage.

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Section: Resultssupporting

confidence: 94%

Fed State Prior to Hemorrhagic Shock and Polytrauma in a Porcine Model Results in Altered Liver Transcriptomic Response

et al. 2014

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“…Structural alterations of the cytoskeleton following ischemia reperfusion have been reported to cause disturbances of intracellular transport processes and cell motility and microcirculation leading to organ dysfunction [ 29 – 32 ]. In liver cells, F-actin is a relevant component of liver cytoskeleton which forms microfilaments involved in intracellular transport processes, such as exocytosis and endocytosis, maintenance of cell shape, and canalicular motility responsible for bile flow [ 25 , 31 , 33 , 34 ]. In this context, we have explored whether PEG 35 pretreatment could maintain the cytoskeleton structure and preserve the morphological characteristics of hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

Polyethylene Glycol Preconditioning: An Effective Strategy to Prevent Liver Ischemia Reperfusion Injury

Béjaoui

Pantazi

Calvo

et al. 2016

Oxidative Medicine and Cellular Longevity

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Hepatic ischemia reperfusion injury (IRI) is an inevitable clinical problem for liver surgery. Polyethylene glycols (PEGs) are water soluble nontoxic polymers that have proven their effectiveness in various in vivo and in vitro models of tissue injury. The present study aims to investigate whether the intravenous administration of a high molecular weight PEG of 35 kDa (PEG 35) could be an effective strategy for rat liver preconditioning against IRI. PEG 35 was intravenously administered at 2 and 10 mg/kg to male Sprague Dawley rats. Then, rats were subjected to one hour of partial ischemia (70%) followed by two hours of reperfusion. The results demonstrated that PEG 35 injected intravenously at 10 mg/kg protected efficiently rat liver against the deleterious effects of IRI. This was evidenced by the significant decrease in transaminases levels and the better preservation of mitochondrial membrane polarization. Also, PEG 35 preserved hepatocyte morphology as reflected by an increased F-actin/G-actin ratio and confocal microscopy findings. In addition, PEG 35 protective mechanisms were correlated with the activation of the prosurvival kinase Akt and the cytoprotective factor AMPK and the inhibition of apoptosis. Thus, PEG may become a suitable agent to attempt pharmacological preconditioning against hepatic IRI.

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“…One of the mechanisms of liver transplantation failure is ischemia-reperfusion type of injury to the transplanted liver. Evidence indicates that ischemia-reperfusion induces alteration in bile canalicular F-actin microfilaments in hepatocytes 94 . Ischemia-reperfusion generates reactive oxygen species, the factors that are likely involved in tight junction disruption and bile duct injury in the transplanted liver.…”

Section: Tight Junction Dysfunction In Biliary Diseasesmentioning

confidence: 99%

Bile duct epithelial tight junctions and barrier function

Rao

Samak

2013

Tissue Barriers

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Bile ducts play a crucial role in the formation and secretion of bile as well as excretion of circulating xenobiotic substances. In addition to its secretory and excretory functions, bile duct epithelium plays an important role in the formation of a barrier to the diffusion of toxic substances from bile into the hepatic interstitial tissue. Disruption of barrier function and toxic injury to liver cells appear to be involved in the pathogenesis of a variety of liver diseases such as primary sclerosing cholangitis, primary biliary cirrhosis and cholangiocarcinoma. Although the investigations into understanding the structure and regulation of tight junctions in gut, renal and endothelial tissues have expanded rapidly, very little is known about the structure and regulation of tight junctions in the bile duct epithelium. In this article we summarize the current understanding of physiology and pathophysiology of bile duct epithelium, the structure and regulation of tight junctions in canaliculi and bile duct epithelia and different mechanisms involved in the regulation of disruption and protection of bile duct epithelial tight junctions. This article will make a case for the need of future investigations toward our understanding of molecular organization and regulation of canalicular and bile duct epithelial tight junctions.

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Untitled

Cited by 27 publications

References 28 publications

Fed State Prior to Hemorrhagic Shock and Polytrauma in a Porcine Model Results in Altered Liver Transcriptomic Response

Fed State Prior to Hemorrhagic Shock and Polytrauma in a Porcine Model Results in Altered Liver Transcriptomic Response

Polyethylene Glycol Preconditioning: An Effective Strategy to Prevent Liver Ischemia Reperfusion Injury

Bile duct epithelial tight junctions and barrier function

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