GNPS - Glutathione adduct_in vitro_human liver microsomes
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive
ORGANISM(S): Homo Sapiens (ncbitaxon:9606)
SUBMITTER: 
Ju-Hyun Kim
PROVIDER: MSV000093215 | GNPS | Wed Nov 01 00:56:00 GMT 2023
REPOSITORIES: GNPS
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Project description:A source of functioning hepatocytes for liver cell transplantation and liver support is in need. hESCs , when transplanted, generally form teratomas. We studied capacity of hESCs to differentiate to hepatocyte like cells under the effect of in vivo liver regeneration. In SCID-Beige mice hepatocyte replication peaked 48 hours after CCl4 injection; 24 hours earlier 106 hESCs or EBs at different stages of differentiation were transplanted into the spleen. Comparisons were made to teratomas formed in the hind limb of untreated animals. RT-PCR and gene microarray were used for liver and human specific markers. Immunohistochemistry to AFP,AAT, ALB, HEP-PAR I AND CK-18,19 were performed. EBs formed a single large teratoma in the spleen and small teratomas in the liver. Expression of PCR- identified liver specific markers was greater in the spleen than in the liver. Adult hepatocyte specific markers were expressed in the hind limb teratoma excised after 7 weeks. When late EBs were transplanted before CCl4 exposure, no teratomas formed. Rather, an abundance of probably undifferentiated ectodermal origin cells presented. In this descriptive study, transplanted early human EBs formed teratomas that differed in size and molecular markers. Within teratomas, the degree of maturation into hepatocytes correlated better with the time duration in vivo than with growth stimulation. Late EBs formed non differentiated ectodermal cells only in a regenerative microenvironment. 4 samples were analyzed. Clean mouse liver used as neg. control. Mouse liver injected with CCl4 and transplanted with late Ebs, tumor was not observed. Two mouse livers injected with CCl4 and transplanted with late Ebs, tumor was observed.
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Metadata Submitted in BioModels by: Zainab Ashimiyu-Abdusalam
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https://github.com/ersilia-os/eos31ve
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Project description:Background & aims: Polycystic liver disease (PLD) is an autosomal dominantly inherited disorder caused by mutations in genes such as PRKCSH and SEC63. It has been thought that cysts develop from biliary progenitor cells due to loss-of-heterozygosity (LOH), leading to aberrant proliferation or defects in differentiation. Cyst expansion can be suppressed by somatostatin analogues such as lanreotide. There is no human in vitro model available that truly recapitulates polycystic liver disease. We hypothesize that PLD progenitors can form bipotent liver organoids that carry key features of cyst development. To find gene expression differences between Human Polycystic Liver Disease and Normal Biliary Stem Cells. Methods: Cells from normal biliary duct (n=6), cyst biliary epithelium (n=60) and cyst fluid (n=31) were isolated and placed under conditions suitable for expansion of human adult liver stem cells. We analyzed genetic LOH, gene expression, differentiation capacity, response to lanreotide and cilium formation of these organoids. Results: Cholangiocytes from cyst biliary epithelium (47/60) and cyst fluid (9/31) proved capable of expanding as bipotent liver organoids. Multiple cyst organoids displayed LOH surrounding PRKCSH or SEC63 regions. Organoids formed cilia when proliferation was inhibited. Neither hepatocyte nor biliary differentiation of PLD organoids was impaired. RNAseq revealed no significantly dysregulated pathway in PLD organoids. Lanreotide significantly decreased expansion of liver organoids in comparison to negative control (197% ± 46% versus 547% ± 28%; p: 0.038). Conclusion & discussion: Biliary progenitor cells from patient cyst epithelium and fluid can expand into liver organoids. They recapitulate key characteristics of PLD, and are a promising human in vitro model for research, diagnostics and treatment of polycystic liver diseases and cholangiociliopathies.
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