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| Research article summary (published 30 Aug 1990): |
Modulation of extracellular matrix components during dimethylnitrosamine-induced cirrhosis.
Full Abstract
Liver fibrosis was induced in rats after administration of dimethylnitrosamine (DMN) intraperitoneally three times a week for 3 weeks. Incomplete septa appeared after 7 days and evidence of nodulation of the parenchyma was observed after 21 days. Both distribution of extracellular matrix components (collagen type I, type III and type IV, laminin, fibronectin, heparan sulphate proteoglycan) and the distribution of desmin as a marker of lipocytes (Ito cells) and of iso-alpha-smooth muscle actin were studied with immunoperoxidase. Changes in the distribution of extracellular matrix components outlined both the formation of septa and the development of nodules with changes in the sinusoidal pattern evoking aspects of capillarization. The number of desmin-positive cells increased in DMN-treated animals, showing a prominent reaction in the fibrous septa. In the normal liver, lipocytes were positive for laminin and negative for actin, but septal and juxta-septal lipocytes were positive for both antigens, suggesting the presence of transitional cells with mixed immunoreactivity. This was confirmed by ultrastructural studies which showed typical intraseptal myofibroblasts and other elements exhibiting the structural features of both myofibroblasts and lipocytes.
Author information
Author/s: Jezequel, A M (AM); Ballardini, G (G); Mancini, R (R); Paolucci, F (F); Bianchi, F B (FB); Orlandi, F (F);
Affiliation: Institute of Experimental Pathology, University of Ancona, Italy.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Journal of hepatology (J Hepatol), published in NETHERLANDS. (Language: eng)
Reference: 1990-Sep; vol 11 (issue 2) : pp 206-14
Dates: Created 1991/01/24; Completed 1991/01/24; Revised 2006/11/15;
PMID: 2254631, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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