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Arch Toxicol. 2017 Nov;91(11):3689-3692. doi: 10.1007/s00204-017-2040-8. Epub 2017 Aug 19.

A frequent misinterpretation in current research on liver fibrosis: the vessel in the center of CCl4-induced pseudolobules is a portal vein.

Author information

1
Molecular Hepatology Section, Department of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. seddik.hammad@medma.uni-heidelberg.de.
2
Department of Forensic Medicine and Veterinary Toxicology, Faculty of Veterinary Medicine, South Valley University, Qena, Egypt. seddik.hammad@medma.uni-heidelberg.de.
3
Department Food Safety, German Federal Institute for Risk Assessment, Berlin, Germany.
4
Molecular Hepatology Section, Department of Medicine II, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
5
Department of Pathology, Faculty of Medicine, Minia University, Minia, Egypt.
6
Leibniz Research Centre for Working Environment and Human Factors, Technical University of Dortmund (IfADo), Dortmund, Germany.

Abstract

Carbon tetrachloride-induced liver injury is a thoroughly studied model for regeneration and fibrosis in rodents. Nevertheless, its pattern of liver fibrosis is frequently misinterpreted as portal type. To clarify this, we show that collagen type IV+ "streets" and α-SMA+ cells accumulate pericentrally and extend to neighbouring central areas of the liver lobule, forming a 'pseudolobule'. Blood vessels in the center of such pseudolobules are portal veins as indicated by the presence of bile duct cells (CK19+) and the absence of pericentral hepatocytes (glutamine synthetase+). It is critical to correctly describe this pattern of fibrosis, particulary for metabolic zonation studies.

KEYWORDS:

CCl4; Liver fibrosis; Pseudolobule

PMID:
28825120
DOI:
10.1007/s00204-017-2040-8
[Indexed for MEDLINE]

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