Abstract
We examined the effect of sodium butyrate on in vitro angiogenesis and cyclooxygenase (COX) expression using primary cultures of human intestinal microvascular endothelial cells (HIMEC). Butyrate inhibited VEGF-induced cellular proliferation, transmigration and tube formation of HIMEC. Butyrate also inhibited COX-2 expression as well as prostaglandin (PG)E2 and PGI2 production, and administration of PGI2 analog partially reversed the effect of butyrate on HIMEC angiogenesis. These results indicate that sodium butyrate inhibits HIMEC angiogenesis through down-regulation of COX-2 expression and PG production, and suggest that anti-angiogenic mechanisms may also be involved in the inhibitory effect of sodium butyrate on tumor growth.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Angiogenesis Inhibitors / pharmacology*
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Butyrates / pharmacology*
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Cell Division / drug effects
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Cell Movement / drug effects
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / pharmacology
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Dinoprostone / biosynthesis
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Drug Antagonism
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Endothelium, Vascular / cytology*
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Endothelium, Vascular / drug effects
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Epoprostenol / biosynthesis
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Humans
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Intestines / blood supply*
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Isoenzymes / biosynthesis
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Isoenzymes / physiology
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Membrane Proteins
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Microcirculation
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Neovascularization, Physiologic / drug effects*
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Prostaglandin-Endoperoxide Synthases / biosynthesis
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Prostaglandin-Endoperoxide Synthases / physiology
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Vascular Endothelial Growth Factor A / pharmacology
Substances
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Angiogenesis Inhibitors
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Butyrates
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Vascular Endothelial Growth Factor A
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Epoprostenol
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Cyclooxygenase 2
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases
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Dinoprostone