Human Liver Development as a Template to Generate High Fidelity Models

Author(s):  
Claire Medine ◽  
Janet Kung ◽  
Catherine Payne ◽  
James Black ◽  
Richard Anderson ◽  
...  
1999 ◽  
Vol 112 (4) ◽  
pp. 277-282 ◽  
Author(s):  
F. Quondamatteo ◽  
T. Knittel ◽  
M. Mehde ◽  
G. Ramadori ◽  
R. Herken

2009 ◽  
Vol 51 (1) ◽  
pp. 114-126 ◽  
Author(s):  
Jean Paul Brizard ◽  
Jeanne Ramos ◽  
Agnés Robert ◽  
Daniel Lafitte ◽  
Nicole Bigi ◽  
...  

1993 ◽  
Vol 71 (5-6) ◽  
pp. 241-247 ◽  
Author(s):  
B. Geetha Devi ◽  
C. M. Habeebullah ◽  
P. D. Gupta

Ontogeny of hepatocyte proliferation inhibitory (HPI) activity was studied during human liver development. HPI activity was first noticed in the cytosolic fraction of 20-week-old fetal liver and thereafter it began to increase with the liver maturation. An inverse correlation between the ontogeny of HPI activity and mitotic counting of the hepatocytes during human liver development was established. The crude HPI fraction from fetal and adult human liver inhibited the incorporation of [3H]thymidine into the DNA of 2-day-old rat liver and HepG2 cells and the inhibitory effect was directly proportional to the age of the HPI source. Prolonged exposure of HepG2 cells to the HPI fraction was also found to be cytotoxic. Preliminary characterization of the crude HPI fraction revealed an age-dependent increase in proteins of 18, 28, and 60 kilodaltons following silver chloride staining of sodium dodecyl sulfate - polyacrylamide gel electrophoresis and densitometric scanning.Key words: human liver, hepatocyte proliferation inhibitor, ontogeny, sodium dodecyl sulfate - polyacrylamide gel electrophoresis, HepG2 cells, cytotoxic.


2019 ◽  
Author(s):  
Tala Mon ◽  
Ogechi Ogoke ◽  
Claire Shamul ◽  
Shatoni Ross ◽  
Saroja Rao ◽  
...  

ABSTRACTLiver organogenesis has thus far served as a paradigm for solid organ formation, and has recently attracted interest due to challenges faced in liver regenerative medicine. Murine genetic studies indicate that early steps in morphogenesis are required, suggesting that three-dimensional imaging of early liver morphogenesis at high resolution can improve our understanding. Unfortunately, existing approaches to image early liver morphogenesis have been unable to achieve high spatial resolution (1-5 um) required. In this study, we focused on imaging, visualization, and analysis of early liver development. We utilized available online databases for both mouse (EMAP) and human (3D Atlas of Human Embryology) liver development. To visualize liver bud morphogenesis at high spatial resolution, we performed 3D reconstructions of stacked, digital tissue sections. We show dynamic 3D hepatic cord formation in the mouse in humans. Interestingly, when we quantified fetal liver growth, we showed that 3D fetal liver growth appears to occur in spurts rather continuously, and 3D images suggest that there could be considerable remodeling during these stages. Further, our analysis of the STM, in both mouse and humans, demonstrates that it increases in size during early fetal liver growth, that is highly interconnecting with liver epithelium, and that it can have strong local effects on growth. Finally, we identify and visualize and identify human hepatic cord formation followed by rapid sheet-like growth, which we propose could be an under-appreciated morphological feature that enables rapid growth of early human fetal liver. These studies will motivate future approaches to employ in vitro culture and organoid technology to improve human PSC differentiation, and improve disease modeling, and therapeutic opportunities for liver diseases. In conclusion, compared to 2D sectioning, high spatial resolution imaging of the mouse and human 3D liver bud morphogenesis enables greatly improved visualization of the hepatic cords, 3D sheet-like liver cell growth, STM-epithelial cell interactions, and quantitative comparisons between mouse and human liver bud morphogenesis.


Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 309-316 ◽  
Author(s):  
T.J. Ekstrom ◽  
H. Cui ◽  
X. Li ◽  
R. Ohlsson

IGF2 has been shown to be expressed preferentially from the paternally derived allele, although the maternal allele can be found active during both prenatal and postnatal development as well as in neoplastic tumours in humans. We addressed here whether or not the biallelic expression patterns that can be seen during postnatal human liver development reflected a coordinated change in the activities of the four promoters of human IGF2. We show here that the P2, P3 and P4 promoters, but not the P1 promoter, display monoallelic activity in embryonic, neonatal and younger infant liver specimens. The P2, P3 and P4 promoters can, however, be found active either monoallelically or biallelically or even monoallelically on opposite parental alleles in older infant and adult liver specimens. In contrast, H19, which is closely linked to IGF2, is monoallelically expressed in all postnatal liver samples analysed. We conclude that the functional imprinting status of IGF2 during postnatal liver development appears to be promoter/enhancer-specific and either partly or completely independent of H19.


2011 ◽  
Vol 54 ◽  
pp. S278-S279
Author(s):  
A. Gumerova ◽  
A. Kiassov ◽  
M. Titova ◽  
S. Abdulkhakov ◽  
M. Kaligin ◽  
...  

Hepatology ◽  
2007 ◽  
Vol 47 (2) ◽  
pp. 719-728 ◽  
Author(s):  
Luca Fabris ◽  
Massimiliano Cadamuro ◽  
Louis Libbrecht ◽  
Peggy Raynaud ◽  
Carlo Spirlì ◽  
...  

1995 ◽  
Vol 108 (4) ◽  
pp. A1161 ◽  
Author(s):  
K. Saito ◽  
S. Spaulding ◽  
Y. Haruna ◽  
M.A. Nalesnik ◽  
M.A. Gerber

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