Characterization and Functional Analyses of Hepatic Mesothelial Cells in Mouse Liver Development

Onitsuka, Izumi; Tanaka, Minoru; Miyajima, Atsushi

doi:10.1053/j.gastro.2009.12.059

Cited by 70 publications

(83 citation statements)

References 24 publications

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“…S3). This may be associated with the recent study showing that the morphogenesis and proliferation of the hepatocytes occur more actively in the peripheral region than in the central region of each liver lobule in the late-organogenicstage embryos (Onitsuka et al, 2010). It is also possible that hepatocytes in the periphery might respond first in an inflammatory response through the vasculatures, because blood flows from the periphery toward the center of each liver lobule.…”

Section: Discussionmentioning

confidence: 83%

Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice

et al. 2013

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SUMMARYCongenital biliary atresia is an incurable disease of newborn infants, of unknown genetic causes, that results in congenital deformation of the gallbladder and biliary duct system. Here, we show that during mouse organogenesis, insufficient SOX17 expression in the gallbladder and bile duct epithelia results in congenital biliary atresia and subsequent acute 'embryonic hepatitis', leading to perinatal death in ~95% of the Sox17 heterozygote neonates in C57BL/6 (B6) background mice. During gallbladder and bile duct development, Sox17 was expressed at the distal edge of the gallbladder primordium. In the Sox17 +/-B6 embryos, gallbladder epithelia were hypoplastic, and some were detached from the luminal wall, leading to bile duct stenosis or atresia. The shredding of the gallbladder epithelia is probably caused by cell-autonomous defects in proliferation and maintenance of the Sox17 +/-gallbladder/bile duct epithelia. Our results suggest that Sox17 plays a dosage-dependent function in the morphogenesis and maturation of gallbladder and bile duct epithelia during the late-organogenic stages, highlighting a novel entry point to the understanding of the etiology and pathogenesis of human congenital biliary atresia.

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Section: Discussionmentioning

confidence: 83%

Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice

et al. 2013

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“…Liver cell subpopulations include such distinct specialized cell types as parenchymal cells or hepatocytes [1] and non-parenchymal cells including, cholangiocytes [2], portal fibroblasts [3], hepatic stellate cells (HSC) [4], mesothelial cells [5], sinusoidal endothelial cells [6], and immune cells [7,8]. For most of these cell types, the establishment of various immortalized cell lines in human and rodent species represents a major experimental advance, providing in vitro models for the study of liver functions in cell-specific manner.…”

Section: Introductionmentioning

confidence: 99%

Expression of mediators of purinergic signaling in human liver cell lines

Goree

Lavoie

Fausther

et al. 2014

Purinergic Signalling

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Purinergic signaling regulates a diverse and biologically relevant group of processes in the liver. However, progress of research into functions regulated by purinergic signals in the liver has been hampered by the complexity of systems probed. Specifically, there are multiple liver cell subpopulations relevant to hepatic functions, and many of these have been effectively modeled in human cell lines. Furthermore, there are more than 20 genes relevant to purinergic signaling, each of which has distinct functions. Hence, we felt the need to categorize genes relevant to purinergic signaling in the best characterized human cell line models of liver cell subpopulations. Therefore, we investigated the expression of adenosine receptor, P2X receptor, P2Y receptor, and ecto-nucleotidase genes via RT-PCR in the following cell lines: LX-2, hTERT, FH11, HepG2, Huh7, H69, and MzChA-1. We believe that our findings will provide an excellent resource to investigators seeking to define functions of purinergic signals in liver physiology and liver disease pathogenesis.

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“…Previous studies have demonstrated that the genes mentioned above and other genes [e.g., glycoprotein m6a, mesothelin, Uroplakin 1β and 3 β, Cyp2s1, mucin 16, crystalline, Prss12, Slipi, Caveolin, Dermokin, Calcitonin-related peptide, vanin, cytokeratin 7, Slc9a3r1, and Slc39a8 (metal ion transporter)], Igfbp6, see Fig. S6) are expressed in hepatic mesothelium (48). Furthermore, the gene expression profiles of epicardium isolated from adult mouse infarction-injured hearts identified the same genes among epicardium-specific signature genes, and for the first time, to our knowledge, implicated these genes (alone or in combination) in wound healing (49).…”

Section: Elastinmentioning

confidence: 99%

Origin of myofibroblasts in the fibrotic liver in mice

Iwaisako

Jiang

Zhang³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

448

461

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Significance Liver resident activated hepatic stellate cells (aHSCs), and activated portal fibroblasts (aPFs) are the major source of the fibrous scar in the liver. aPFs have been implicated in liver fibrosis caused by cholestatic liver injury, whereas fibrosis in hepatotoxic liver injury is attributed to aHSCs. However, the contribution of aPFs to cholestatic fibrosis is not well characterized because of difficulties in cell purification and the lack of identified aPF-specific markers. We have developed a novel flow cytometry-based method of aPFs purification from the nonparenchymal cell fraction of collagen-α1(I)-GFP mice and have identified potential aPF-specific markers. The goal of this study is to determine whether aPFs contribute to cholestatic liver fibrosis and identify the mechanism(s) of their activation.

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Characterization and Functional Analyses of Hepatic Mesothelial Cells in Mouse Liver Development

Cited by 70 publications

References 24 publications

Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice

Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice

Expression of mediators of purinergic signaling in human liver cell lines

Origin of myofibroblasts in the fibrotic liver in mice

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