Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-12-22
pubmed:abstractText
Activation of liver progenitor cells was studied in rat liver induced to regenerate after carbon tetrachloride (CCl4) or D-galactosamine (GalN) injury. A change in the concentration of histone-3 mRNA was used as a marker for cell proliferation and the fetal form of alpha-fetoprotein (AFP) mRNA as a marker for fetal hepatoblasts. gamma-Glutamyltranspeptidase (GGT) and glutathione-S-transferase P were used as markers for activation of putative liver progenitor cells. After CCl4 administration, the proliferative response was high but confined primarily to parenchymal cells. No changes in the relative expression of albumin, glutathione-S-transferase P or insulin-like growth factor-II were observed. On the other hand, the level of AFP mRNA was increased modestly and predominantly in the nonparenchymal cell (NPC) fraction. After GalN administration, proliferation of NPC began within 24 hr, primarily in the portal area around the bile ducts. Activated cells were bile "duct-like" in appearance, had scant cytoplasm, and a pale, oval-shaped nucleus. On Day 2, they formed rows and clusters, expanding from the portal zone and invading the parenchyma, as well as proliferating in regions of focal necrosis. On Days 3 and 5, NPC expressing histone-3 mRNA expanded further, forming pseudoducts and islet-like structures (NPC structures) throughout the hepatic lobule. Proliferating NPC were positive for GGT. Some GGT-positive cells on Days 3 and 5 were also positive for fetal AFP mRNA. Expression of fetal AFP mRNA lagged behind that of GGT by 24 hr, was highest on Day 5, and then declined. Expression of albumin mRNA and glucose 6-phosphatase decreased during the first 48 hr after GalN administration and then resumed. These findings indicate that after GalN injury, the liver responds with activation of putative progenitor cells that proliferate and then differentiate through the hepatocyte lineage, whereas the regenerative response after CCl4 administration is primarily through proliferation of preexisting hepatocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0037-9727
pubmed:author
pubmed:issnType
Print
pubmed:volume
204
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
242-52
pubmed:dateRevised
2007-11-2
pubmed:meshHeading
pubmed-meshheading:7694303-Albumins, pubmed-meshheading:7694303-Animals, pubmed-meshheading:7694303-Carbon Tetrachloride Poisoning, pubmed-meshheading:7694303-Galactosamine, pubmed-meshheading:7694303-Gene Expression, pubmed-meshheading:7694303-Glutathione Transferase, pubmed-meshheading:7694303-Histones, pubmed-meshheading:7694303-In Situ Hybridization, pubmed-meshheading:7694303-Insulin-Like Growth Factor II, pubmed-meshheading:7694303-Liver, pubmed-meshheading:7694303-Liver Regeneration, pubmed-meshheading:7694303-Male, pubmed-meshheading:7694303-RNA, Messenger, pubmed-meshheading:7694303-Rats, pubmed-meshheading:7694303-Rats, Inbred F344, pubmed-meshheading:7694303-Rats, Inbred Lew, pubmed-meshheading:7694303-Rats, Sprague-Dawley, pubmed-meshheading:7694303-Stem Cells, pubmed-meshheading:7694303-alpha-Fetoproteins
pubmed:year
1993
pubmed:articleTitle
Models for hepatic progenitor cell activation.
pubmed:affiliation
Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461.
pubmed:publicationType
Journal Article