ArticleJournal of molecular histology2006
Influx of macrophages into livers of rats treated with hepatotoxicants (thioacetamide, allyl alcohol, D-galactosamine) induces expression of HSP25.
Article in Journal of molecular histology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Serum levels of anti-heat shock protein 27 antibodies in patients with chronic liver disease.Cell stress & chaperones · 2021Article
- Immunodetection of cyclooxygenase-2 (COX-2) is restricted to tissue macrophages in normal rat liver and to recruited mononuclear phagocytes in liver injury and cholangiocarcinoma.Histochemistry and cell biology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment of rats with a single dose of thioacetamide (TAA) provokes centrilobular inflammation and a significant expression of heat shock protein HSP25 in hepatocytes surrounding the area of inflammation. The HSP25 accumulation in hepatocytes adjacent to inflammatory regions was confirmed by identification of positive hepatocytes concentrated at periportal areas after treatment of rats with allyl alcohol (AA) or distributed diffusely throughout liver lobule after treatment with D-galactosamine (D-gal). In our model of TAA-treated rats the use of the anti-inflammatory drug-indomethacin, and the redox-regulating drug-N-acetylcysteine (NAC), significantly attenuated TAA-induced HSP25 expression and evoked morphological changes of recruited ED1+ macrophages. Treatment of rats with gadolinium chloride (GdCl(3)) decreased considerably the number of Kupffer cells (ED2+ macrophages) without affecting significantly the number and morphology of ED1+ macrophages as well as the expression pattern of TAA-induced HSP25. Our data shows for the first time that ED1+ macrophages recruited into the liver by treatment with TAA play a significant role in HSP25 induction in hepatocytes.
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