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Monocyte chemoattractant protein (MCP‐1) is expressed in human cardiac cells and is differentially regulated by inflammatory mediators and hypoxia
Author(s) -
Hohensinner Philipp J.,
Kaun Christoph,
Rychli Kathrin,
Ben-Tal Cohen Enbal,
Kastl Stefan P.,
Demyanets Svitlana,
Pfaffenberger Stefan,
Speidl Walter S.,
Rega Gersina,
Ullrich Robert,
Maurer Gerald,
Huber Kurt,
Wojta Johann
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.05.043
Subject(s) - chemokine , monocyte , inflammation , hypoxia (environmental) , downregulation and upregulation , ccl2 , chemotaxis , immunology , microbiology and biotechnology , myocardial infarction , chemistry , medicine , biology , receptor , biochemistry , gene , organic chemistry , oxygen
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.