scholarly journals Liver Progenitors and Adult Cell Plasticity in Hepatic Injury and Repair: Knowns and Unknowns

2020 ◽  
Vol 15 (1) ◽  
pp. 23-50 ◽  
Author(s):  
Sungjin Ko ◽  
Jacquelyn O. Russell ◽  
Laura M. Molina ◽  
Satdarshan P. Monga
Keyword(s):  
Liver Injury ◽  
Epithelial Cells ◽  
Progenitor Cells ◽  
Experimental Models ◽  
Acute Injury ◽  
Biliary Epithelial Cells ◽  
Adult Cell ◽  
Life Threatening ◽  
Injury And Repair ◽  
End Stage

The liver is a complex organ performing numerous vital physiological functions. For that reason, it possesses immense regenerative potential. The capacity for repair is largely attributable to the ability of its differentiated epithelial cells, hepatocytes and biliary epithelial cells, to proliferate after injury. However, in cases of extreme acute injury or prolonged chronic insult, the liver may fail to regenerate or do so suboptimally. This often results in life-threatening end-stage liver disease for which liver transplantation is the only effective treatment. In many forms of liver injury, bipotent liver progenitor cells are theorized to be activated as an additional tier of liver repair. However, the existence, origin, fate, activation, and contribution to regeneration of liver progenitor cells is hotly debated, especially since hepatocytes and biliary epithelial cells themselves may serve as facultative stem cells for one another during severe liver injury. Here, we discuss the evidence both supporting and refuting the existence of liver progenitor cells in a variety of experimental models. We also debate the validity of developing therapies harnessing the capabilities of these cells as potential treatments for patients with severe and chronic liver diseases.

scholarly journals YAP, but Not RSPO-LGR4/5, Signaling in Biliary Epithelial Cells Promotes a Ductular Reaction in Response to Liver Injury

2019 ◽  
Vol 25 (1) ◽  
pp. 39-53.e10 ◽  
Author(s):  
Lara Planas-Paz ◽  
Tianliang Sun ◽  
Monika Pikiolek ◽  
Nadire R. Cochran ◽  
Sebastian Bergling ◽  
...  
Keyword(s):  
Liver Injury ◽  
Epithelial Cells ◽  
Ductular Reaction ◽  
Biliary Epithelial Cells

145 Enhanced TLR Signaling Breaks Endotoxin Tolerance in Human Biliary Epithelial Cells in END-Stage Chronic Inflammatory Liver Disease

2009 ◽  
Vol 136 (5) ◽  
pp. A-28
Author(s):  
Tobias Mueller ◽  
Andreas Pascher ◽  
Peter Neuhaus ◽  
Bertram Wiedenmann ◽  
Thomas Berg
Keyword(s):  
Liver Disease ◽  
Epithelial Cells ◽  
Endotoxin Tolerance ◽  
Tlr Signaling ◽  
Biliary Epithelial Cells ◽  
End Stage

scholarly journals Chronic Liver Injury Induces Conversion of Biliary Epithelial Cells into Hepatocytes

2018 ◽  
Vol 23 (1) ◽  
pp. 114-122.e3 ◽  
Author(s):  
Xing Deng ◽  
Xin Zhang ◽  
Weiping Li ◽  
Ren-Xin Feng ◽  
Lu Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Epithelial Cells ◽  
Chronic Liver ◽  
Chronic Liver Injury ◽  
Biliary Epithelial Cells

Presence of markers for liver progenitor cells in human-derived intrahepatic biliary epithelial cells

2004 ◽  
Vol 24 (6) ◽  
pp. 669-678 ◽  
Author(s):  
Chao Liu ◽  
Thomas Schreiter ◽  
Olaf Dirsch ◽  
Guido Gerken ◽  
Karl J. Oldhafer ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Progenitor Cells ◽  
Biliary Epithelial Cells

Toll-like receptor-4 expression by hepatic progenitor cells and biliary epithelial cells in HCV-related chronic liver disease

2011 ◽  
Vol 25 (4) ◽  
pp. 576-589 ◽  
Author(s):  
Umberto Vespasiani-Gentilucci ◽  
Simone Carotti ◽  
Andrea Onetti-Muda ◽  
Giuseppe Perrone ◽  
Stefano Ginanni-Corradini ◽  
...  
Keyword(s):  
Liver Disease ◽  
Epithelial Cells ◽  
Chronic Liver Disease ◽  
Progenitor Cells ◽  
Chronic Liver ◽  
Hepatic Progenitor Cells ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Biliary Epithelial Cells

Plasminogen directs the pleiotropic effects of uPA in liver injury and repair

2003 ◽  
Vol 284 (3) ◽  
pp. G508-G515 ◽  
Author(s):  
Angela R. Currier ◽  
Gregg Sabla ◽  
Stephanie Locaputo ◽  
Hector Melin-Aldana ◽  
Jay L. Degen ◽  
...  
Keyword(s):  
Liver Injury ◽  
Transgenic Mice ◽  
Molecular Mechanisms ◽  
Acute Injury ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Regenerative Nodules ◽  
Liver Repair ◽  
Injury And Repair

The urokinase-type plasminogen activator (uPA) plays a central role in liver repair. Nevertheless, the hepatic overexpression of uPA results in panlobular injury and neonatal mortality. Here, we define the molecular mechanisms of liver injury and explore whether uPA can regulate liver repair independently of plasminogen. To address the hypothesis that the liver injury in transgenic mice results from the intracellular activation of plasminogen by transgene-derived uPA (uPAT), we generated mice that overexpress uPAT and lack functional plasminogen (uPAT-Plg−). In these mice, loss of plasminogen abolished the hepatocyte-specific injury and prevented the formation of regenerative nodules displayed by uPAT littermates. Despite the increased expression of hepatic uPA, livers of uPAT-Plg−mice were unable to clear necrotic cells and restore normal lobular organization after an acute injury. Notably, high levels of circulating uPA in uPAT-Plg−mice did not prevent the long-term extrahepatic abnormalities previously associated with plasminogen deficiency. These data demonstrate that plasminogen directs the hepatocyte injury induced by uPAT and mediates the reparative properties of uPA in the liver.

Ultrastructural Changes Associated with Alcoholic Hyalin in Hepatocytes and Biliary Epithelial Cells

1971 ◽  
Vol 29 ◽  
pp. 572-573
Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo ◽  
Fawzia Batti
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Liver Biopsy ◽  
Alcoholic Hepatitis ◽  
Ultrastructural Changes ◽  
Main Mass ◽  
Biliary Epithelial Cells ◽  
Biopsy Specimens ◽  
Alcoholic Hyalin

To learn more of the nature and origin of alcoholic hyalin (AH), 15 liver biopsy specimens from patients with alcoholic hepatitis were studied in detail.AH was found not only in hepatocytes but also in ductular cells (Figs. 1 and 2), although in the latter location only rarely. The bulk of AH consisted of a randomly oriented network of closely packed filaments measuring about 150 Å in width. Bundles of filaments smaller in diameter (40-90 Å) were observed along the periphery of the main mass (Fig. 1), often surrounding it in a rim-like fashion. Fine filaments were also found close to the nucleus in both hepatocytes and biliary epithelial cells, the latter even though characteristic AH was not present (Figs. 3 and 4). Dispersed among the larger filaments were glycogen, RNA particles and profiles of endoplasmic reticulum. Dilated cisternae of endoplasmic reticulum were often conspicuous around the periphery of the AH mass. A limiting membrane was not observed.

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