Why the study?
Do inflammatory cytokines and hypoxia regulate MCP-1 expression in cultured human cardiac cells?
Do inflammatory cytokines and hypoxia regulate MCP-1 expression in cultured human cardiac cells?
In cultured human cardiac cells, MCP-1 expression is driven by inflammatory cytokines rather than hypoxia, suggesting inflammation is the primary trigger for monocyte recruitment in the human heart.
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Suggests inflammation, not hypoxia, drives cardiac MCP-1 in vitro; leaves open in vivo relevance and clinical translation.
The chemokine MCP-1 is thought to play a key role - among many other pathophysiological processes - in myocardial infarction. MCP-1 is not only a key attractant for monocytes and macrophages and as such responsible for inflammation but might also be directly involved in the modulation of repair processes in the heart. We show that cultured human cardiac cells express MCP-1 and that its expression is upregulated by inflammatory cytokines and downregulated by hypoxia. We hypothesize that inflammation but not hypoxia is the main trigger for monocyte recruitment in the human heart.
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Hohensinner et al. (2006) studied this question.
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