A frequent misinterpretation in current research on liver fibrosis: the vessel in the center of CCl4-induced pseudolobules is a portal vein
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 pericentral...
Gespeichert in:
| Hauptverfasser: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2017
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| In: |
Archives of toxicology
Year: 2017, Jahrgang: 91, Heft: 11, Pages: 3689-3692 |
| ISSN: | 1432-0738 |
| DOI: | 10.1007/s00204-017-2040-8 |
| Online-Zugang: | Verlag, Volltext: http://dx.doi.org/10.1007/s00204-017-2040-8 Verlag, Volltext: http://link.springer.com/article/10.1007/s00204-017-2040-8 
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| Verfasserangaben: | Seddik Hammad, Albert Braeuning, Christoph Meyer, Fatma El Zahraa Ammar Mohamed, Jan G. Hengstler, Steven Dooley |
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| 520 | |a 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. | ||
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