Immunolocalization of heparinbinding growth factors (HBGF) types 1 and 2 in rat liver. Selective hyperexpression of HBGF-2 in carbon tetrachloride-induced fibrosis
| Autor: | Jean Rosenbaum, Frederic Charlotte, Khin Maung Win, Elie Serge Zafrani, Daniel Dhumeaux, Anne-Marie Preaux, Philippe Mavier |
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| Rok vydání: | 1993 |
| Předmět: |
Male
Pathology medicine.medical_specialty CCL4 Biology Liver Cirrhosis Experimental digestive system Pathology and Forensic Medicine Rats Sprague-Dawley chemistry.chemical_compound In vivo Fibrosis medicine Animals Carbon Tetrachloride Cellular localization medicine.disease Immunohistochemistry Rats Cell biology Fibroblast Growth Factors Liver chemistry Carbon tetrachloride Hepatic stellate cell Fibroblast Growth Factor 1 Fibroblast Growth Factor 2 Hepatic fibrosis |
| Zdroj: | The Journal of Pathology. 169:471-476 |
| ISSN: | 1096-9896 0022-3417 |
| DOI: | 10.1002/path.1711690414 |
| Popis: | Ito cells play a major role in liver fibrosis but the mechanisms controlling their activation in vivo are poorly understood. Heparin-binding growth factors (HBGF) types 1 and 2 are mitogenic for cultured Ito cells. They have been found in liver extracts but their cellular localization is unknown. We have studied by immunohistochemistry HBGF-1 and -2 expression in normal rat liver and in carbon tetrachloride (CCl4)-induced fibrosis. In normal liver, HBGF-1 was present only in sinusoidal cells whereas HBGF-2 was also detected in endothelial cells lining major vessels. At the acute stage of CCl4 intoxication, HBGF-2 was expressed in centrilobular clusters of mononuclear phagocytes that were surrounded by many HBGF-2-negative Ito cells. In the later stages, HBGF-2 was expressed by Ito cells within the fibrous bands. No modulation of HBGF-1 expression was noted at any stage. These results suggest that (1) at the acute stage of CCl4 intoxication, HBGF-2 produced by mononuclear phagocytes could participate in the recruitment of Ito cells; and (2) during the CCl4-induced fibrotic process, HBGF-2 could contribute to Ito cell proliferation and the synthesis of fibrosis components. In this in vivo model of hepatic fibrosis, the hyperexpression of HBGF-2 is a relatively specific event since the expression of a structurally related molecule, HBGF-1 was not modulated. |
| Databáze: | OpenAIRE |
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