Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6
Autor: | Jozsef Dudas, Giuliano Ramadori, K. Tron, Thomas Kietzmann, Anatoly Samoylenko, R. Novosyadlyy |
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Rok vydání: | 2005 |
Předmět: |
Male
medicine.medical_specialty Pathology Kupffer Cells Turpentine medicine.medical_treatment Inflammation Enzyme-Linked Immunosorbent Assay In situ hybridization Biology Injections Intramuscular Gene Expression Regulation Enzymologic Pathology and Forensic Medicine Western blot Internal medicine medicine Animals Northern blot RNA Messenger Rats Wistar Interleukin 6 Acute-Phase Reaction Muscle Skeletal Molecular Biology Cells Cultured medicine.diagnostic_test Interleukin-6 Acute-phase protein Cell Biology Rats Up-Regulation Heme oxygenase Endocrinology Cytokine Heme Oxygenase (Decyclizing) biology.protein Hepatocytes medicine.symptom Chemical and Drug Induced Liver Injury Heme Oxygenase-1 |
Zdroj: | Laboratory investigation; a journal of technical methods and pathology. 85(3) |
ISSN: | 0023-6837 |
Popis: | Heme oxygenase-1 (HO-1) is the inducible isoform of an enzyme family responsible for heme degradation and was suggested to be involved in the acute phase response in the liver. However, the mechanisms of the HO-1 regulation under inflammatory conditions are poorly understood. Therefore, the purpose of the current work was to study the expression of HO-1 in the liver and other organs of rats with a localized inflammation after intramuscular injection of turpentine oil (TO). Since interleukin-6 (IL-6) is known to be a principal mediator of inflammation, the levels of this cytokine were also estimated in the animal model used. HO-1 and IL-6 expression was evaluated by Northern blot, in situ hybridization, Western blot, immunohistochemistry and enzyme-linked immunosorbent assay. In the liver and injured muscle, the HO-1 mRNA levels were dramatically increased 4-6 h after TO administration. HO-1 protein levels in the liver were elevated starting from 6-12 h after the treatment. In other internal organs such as the heart, kidney and large intestine, only a slight induction of HO-1 mRNA was observed. IL-6-specific transcripts appeared only in the injured muscle and were in accordance with serum levels of IL-6. In turn, temporal expression of IL-6 in the muscle and circulatory IL-6 levels correlated well with HO-1 expression in the liver and injured muscle. In the liver of control rats HO-1 protein was detected in Kupffer cells, while in TO-injected rats also hepatocytes became strongly HO-1 positive. Conversely, in the injured muscle, HO-1 immunoreactivity was attributed only to macrophages. Our data demonstrate that during localized inflammation HO-1 expression was rapidly and strongly induced in macrophages of injured muscle and in hepatocytes, and IL-6 derived from injured muscle seems to be responsible for the HO-1 induction in the liver. |
Databáze: | OpenAIRE |
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