Abstract | AIM:
Oncostatin-M, a member of the gp 130 family of cytokines, has been associated with inflammation, connective tissue production, and extracellular matrix turnover. Since the reperfused heart is associated with an intense inflammatory reaction followed by scar formation, we tested the hypothesis that oncostatin-M is upregulated in response to cardiac injury and may play a part in cardiac repair. METHODS: RESULTS:
Oncostatin-M mRNA expression was detected in ischemic segments within the first 3 h of reperfusion and was persistent over the whole observation period. At the early time points, infiltrating and endothelial cells were the primary source of oncostatin-M mRNA expression. At later time points, macrophages and myofibroblasts were the main contributors. We previously demonstrated in vivo that monocyte-chemoattractant-protein (MCP-1) mRNA is induced early after reperfusion. We stimulated isolated endothelial cells with oncostatin-M and postischemic lymph, which have both upregulated MCP-1 expression in endothelial cells. In addition, isolated fibroblasts stimulated with oncostatin-M demonstrated a dose-dependent proliferative response. CONCLUSION:
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Authors | Marianne Gwechenberger, Deddo Moertl, Richard Pacher, Martin Huelsmann |
Journal | Croatian medical journal
(Croat Med J)
Vol. 45
Issue 2
Pg. 149-57
(Apr 2004)
ISSN: 0353-9504 [Print] Croatia |
PMID | 15103750
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
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Topics |
- Animals
- Cell Division
- Cells, Cultured
- Dogs
- Endothelial Cells
(metabolism, pathology)
- Fibroblasts
(metabolism)
- Immunohistochemistry
- In Situ Hybridization
- Myocardial Ischemia
(metabolism, pathology)
- Myocardial Reperfusion Injury
(metabolism, pathology)
- Oncostatin M
- Peptides
(metabolism)
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