Lack of Abcc3 expression impairs bile-acid induced liver growth and delays hepatic regeneration after partial hepatectomy in mice

Fernández‐Barrena, Maite G.; Monte, María J.; Latasa, María U.; Uriarte, Iker; Vicente, Eva; Chang, Haisul C Y; Rodríguez‐Ortigosa, Carlos M.; Elferink, Ronald Oude; Berasain, Carmen; Marin, José J.G.; Prieto, Jesús; Ávila, Matías A.

doi:10.1016/j.jhep.2011.05.031

Cited by 41 publications

(27 citation statements)

References 29 publications

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“…Instead, reconjugation to taurine or glycine is carried out almost quantitatively by the hepatocyte after the unconjugated bile acid has returned to the liver in the portal circulation, a cycle termed "damage and repair" by Hofmann and Hagey ( 20 ). Although N-acyl amidation does not occur, bile acids do undergo limited phase II transporter, multidrug resistance protein (MRP3) ( ABCC3 ) ( 93 ) ( 94,95 ), but under supraphysiological conditions, such as feeding a diet containing cholic acid, MRP3 appeared to be a more important contributor ( 96 ). The contribution of human MRP3 to intestinal bile acid transport has not been studied directly.…”

Section: Enterocyte Metabolism Of Bile Acidsmentioning

confidence: 99%

Intestinal transport and metabolism of bile acids

Dawson

Karpen

2015

Journal of Lipid Research

449

371

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Section: Enterocyte Metabolism Of Bile Acidsmentioning

confidence: 99%

Intestinal transport and metabolism of bile acids

Dawson

Karpen

2015

Journal of Lipid Research

449

371

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“…Based on a wealth of studies, including genetically modified mouse models, it was postulated that the innate immune system would ''prime'' hepatocytes to respond to the mitogenic action of growth factors, while fluctuations in the levels of key metabolites such as glucose, fatty acids and triglycerides, amino acids and its derivatives such as S-adenosylmethionine, and particularly bile acids would contribute to the onset and termination of the regenerative response after partial liver resection [128][129][130][131][132][133][134][135][136][137]. Nuclear receptors such as PPARa, PPARc, CAR, LXR and the bile acid receptor, FXR, are increasingly recognized as modulators of hepatocyte proliferation during liver regeneration.…”

Section: Regulation Of Hepatocellular Quiescence and Proliferationmentioning

confidence: 99%

Regulation of hepatocyte identity and quiescence

Berasain

Avila

2015

Cell. Mol. Life Sci.

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The liver is a highly differentiated organ with a central role in metabolism, detoxification and systemic homeostasis. To perform its multiple tasks, liver parenchymal cells, the hepatocytes, express a large complement of enabling genes defining their complex phenotype. This phenotype is progressively acquired during fetal development and needs to be maintained in adulthood to guarantee the individual's survival. Upon injury or loss of functional mass, the liver displays an extraordinary regenerative response, mainly based on the proliferation of hepatocytes which otherwise are long-lived quiescent cells. Increasing observations suggest that loss of hepatocellular differentiation and quiescence underlie liver malfunction in chronic liver disease and pave the way for hepatocellular carcinoma development. Here, we briefly review the essential mechanisms leading to the acquisition of liver maturity. We also identify the key molecular factors involved in the preservation of hepatocellular homeostasis and finally discuss potential strategies to preserve liver identity and function.

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“…Previous data have also confirmed the essential roles of BA and FXR in lipid metabolism [34][35][36]. In addtion the modulation of BA flux seems essential for liver regeneration to proceed normally [37]. Overall, bile acid-activated FXR controls bile acid homeostasis.…”

Section: Discussionmentioning

confidence: 68%

Selection of Hepatocyte-Like Cells from Mouse Differentiated Embryonic Stem Cells and Application in Therapeutic Liver Repopulation

Deng

Qiu

et al. 2012

Cell Physiol Biochem

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Backgroud/Aim: Because of the oncogenic risk, it is important to gain the homogeneous and purified cells from differentiated ESCs before transplantation. Here, we aim to select hepatocyte-like cells from differentiated ESCs, and investigate their growth, differentiation and neoplastic formation after intrahepatic transplantation. Methods: Mouse ESCs were primarily induced by Dexamethesone, FGF-4 and HGF sequentially, then placed to a conditioning selection media consisting of 5% cholestatic sera and cultivated for 2 wks. After labeled by CFDA-SE, the selected cells were transplanted into mouse liver in therapeutic liver repopulation models. Results: In the early stage of screening cultivation, most cells were suffered from apoptosis or even death. 1w later, some hepatocyte-like colony-forming units were observed, then the selected cells could grow and tend to be more mature, as assessed by morphological and functional tests. After intrahepatic transplantation, the labeled cells could proliferate and expressed albumin. Moreover, teratoma didn’t form over 3 months. Conclusion: Our conditioning selection media could not only effectively select hepatocyte-like cells from differentiated ESCs, but further promote their growth and differentiation as well. After intrahepatic transplantation in therapeutic liver repopulation models, the selected cells could grow, differentiate and keep partial hepatic function. In particular, the transplantation was safe.

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Lack of Abcc3 expression impairs bile-acid induced liver growth and delays hepatic regeneration after partial hepatectomy in mice

Cited by 41 publications

References 29 publications

Intestinal transport and metabolism of bile acids

Intestinal transport and metabolism of bile acids

Regulation of hepatocyte identity and quiescence

Selection of Hepatocyte-Like Cells from Mouse Differentiated Embryonic Stem Cells and Application in Therapeutic Liver Repopulation

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