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Curcumin modulates hemeoxygenase‐1, eNOS, and endothelial cell cycle progression
Author(s) -
Jackson Steven J. T.,
Venema Richard C.,
Murphy Laura L.,
Singletary Keith W.,
Young Andrew J.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.541.9
Subject(s) - enos , angiogenesis , curcumin , downregulation and upregulation , cell growth , microbiology and biotechnology , endothelial stem cell , cell cycle , chemistry , wound healing , cancer research , cell , biology , nitric oxide , endocrinology , immunology , biochemistry , in vitro , nitric oxide synthase , gene
Curcumin (CMN), a component of turmeric spice that imparts flavor and color to curry, is a known anti‐inflammatory and angiogenesis‐suppressing bioactive agent. Here, we provide the first evidence that CMN inhibits proliferation of endothelial cells, while modulating hemeoxygenase‐1 (HO‐1) and eNOS protein expression. Exposure of non‐confluent bovine aortic endothelial (BAE) cells to CMN, at concentrations as low as 2 μM, resulted in suppressed proliferation, upregulated HO‐1, and downregulated eNOS within 24 h. In confluent cells, HO‐1 protein was similarly upregulated, while eNOS expression was unaffected by CMN. Concentrations of CMN in excess of 5 μM triggered G2/M cell cycle block in non‐confluent BAE cells, while 15 μM CMN clearly disrupted microtubule polymerization. Taken together, these findings indicate differential effects of CMN in cycling vs. noncycling endothelial cells, with potential dose‐dependent implications for wound healing related to endothelial tissue growth and repair. (Supported by USAMRMC)