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Please use this identifier to cite or link to this item: http://dspace.utalca.cl/handle/1950/10177

Title: A New Isoxazolic Compound Acts as alpha 7 Nicotinic Receptor Agonist in Human Umbilical Vein Endothelial Cells
Authors: Cortes, MP.
Alvarez, R.
Sepulveda, E.
Jimenez-Aspee, F.
Astudillo, L.
Vallejos, G.
Gutierrez, M.
Keywords: alpha 7 Nicotinic Receptor
Cytosolic Calcium Signal
Issue Date: Jul-2014
Abstract: Recent evidence suggests that the alpha 7 nicotinic acetylcholine receptors (alpha 7 nAChRs) participate in the development of angiogenesis and could be a new endothelial target for revascularization in therapeutic angiogenesis. It has been shown that in human umbilical vein endothelial cells (HUVECs) alpha 7 nAChR agonists increase the intracellular calcium concentration ([Ca2+](i)), thus inducing proliferation and vessel formation which are important stages of angiogenesis. In the present study we evaluated the effect of new isoxazole compounds on the cytosolic Ca2+ signal in HUVECs using the fluorescent Ca2+ indicator Fluo-3AM and probing the involvement of alpha 7 nAChR by means of pharmacological tools. HUVECs expressed mainly alpha 7 nAChR, since there was no significant difference in the increase in [Ca2+](i) induced by nicotine, a non-selective nicotinic agonist, in relation to choline, a selective alpha 7 nAChR agonist. The increase in [Ca2+](i) induced by 1 mm choline was inhibited significantly (p = 0.014) in cells which had been pre-incubated for 15 mm with methylly-caconitine (MLA), a selective alpha 7 nAChR antagonist. The studied compounds 1, 2, and 3 induced an increase in [Ca2+](i) in a dose-dependent manner. Compound 1 at 10 mu M induced a greater increase in [Ca2+](i) than compounds 2 and 3. The increase in [Ca2+](i) induced by compound 1 was significantly inhibited by MLA (p = 0.013) and completely inhibited by mecamylamine, a non-selective nAChR antagonist, indicating that the isoxazolic compound 1 acts as an alpha 7 nAChR agonist.
Description: Univ Talca, Inst Quim Recursos Nat, Lab Sintesis Organ, Talca, Chile. Astudillo, L (Astudillo, Luis)
URI: http://dspace.utalca.cl/handle/1950/10177
ISSN: 0939-5075
Appears in Collections:Artículos en publicaciones ISI - Universidad de Talca

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