Copper chelator ATN-224 inhibits endothelial function by multiple mechanisms

Copper is required for the proliferation of endothelial cells and copper-lowering therapy reduces tumour growth in animal models. It has been reported that ATN-224, a novel copper chelator, potently inhibits the activity of the copper-dependent enzyme superoxide dismutase 1 (SOD1) in endothelial cel...

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Vydáno v:	Microvascular research Ročník 77; číslo 3; s. 314 - 326
Hlavní autoři:	Lowndes, Sarah A., Sheldon, Helen V., Cai, Shijie, Taylor, Jennifer M., Harris, Adrian L.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Elsevier Inc 01.05.2009
Témata:	Angiogenesis AQP1 ATN-224 Chelating Agents - pharmacology Chelation Therapy Copper chelation Down-Regulation Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Enzyme Inhibitors - pharmacology Gene Silencing Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism HO-1 Humans Microarray Analysis Molybdenum - pharmacology Neovascularization, Physiologic - genetics Pericytes - drug effects Pericytes - pathology RNA Interference RNA, Messenger - metabolism RNA, Small Interfering - genetics RNA, Small Interfering - metabolism SOD1 Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Transfection Up-Regulation SDF-1 CXCR4 HO-1 FACS NRF1 ATN-224 RHAMM AQP1 Angiogenesis BT HUVEC qPCR PBS PEG-SOD RNAi ANGP2 FGF Copper chelation GPX3 IL-1 PGES2 TXNRD1 VEGF GSR siRNA SOD2 KLF2 SOD1 FCS TM ITB4
ISSN:	0026-2862, 1095-9319, 1095-9319
On-line přístup:	Získat plný text
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