Antiangiogenic, antimigratory and antiinflammatory effects of 2-methoxyestradiol in zebrafish larvae
Author
dc.contributor.author
Quezada, Marisol
Author
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Alvarez, Marjorie
es_CL
Author
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Peña, Oscar A.
es_CL
Author
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Henríquez, Soledad
es_CL
Author
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Alençon, Claudia A. d'
es_CL
Author
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Lange, Soledad
es_CL
Author
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Oliva, Barbara
es_CL
Author
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Owen, Gareth I.
es_CL
Author
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Allende Connelly, Miguel
es_CL
Admission date
dc.date.accessioned
2014-01-29T20:06:05Z
Available date
dc.date.available
2014-01-29T20:06:05Z
Publication date
dc.date.issued
2012-11-07
Cita de ítem
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Comparative Biochemistry and Physiology, Part C 157 (2013) 141–149
en_US
Identifier
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doi: 10.1016/j.cbpc.2012.10.008
Identifier
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https://repositorio.uchile.cl/handle/2250/119735
General note
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Artículo de publicación ISI.
en_US
Abstract
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2-Methoxyestradiol (2ME), an endogenous metabolite of 17β-estradiol, has been previously reported to possess
antiangiogenic and antitumor properties. Herein, we demonstrate that the effects of this antiangiogenic
steroid can be readily assayed in live zebrafish, introducing a convenient and robust new model system as a
screening tool for both single cell and collective cell migration assays. Using the in vitro mammalian endothelial
cell line EA.hy926, we first show that cell migration and angiogenesis, as estimated by wound assay and
tube formation respectively, are antagonized by 2ME. In zebrafish (Danio rerio) larvae, dose-dependent exposure
to 2ME diminishes (1) larval angiogenesis, (2) leukocyte recruitment to damaged lateral line neuromasts
and (3) retards the lateral line primordium in its migration along the body. Our results indicate that 2ME has
an effect on collective cell migration in vivo as well as previously reported anti-tumorigenic activity and suggests
that the molecular mechanisms governing cell migration in a variety of contexts are conserved between
fish and mammals. Moreover, we exemplify the versatility of the zebrafish larvae for testing diverse physiological
processes and screening for antiangiogenic and antimigratory drugs in vivo.
en_US
Patrocinador
dc.description.sponsorship
GIO was supported by the BRMC CTU06.
MA was supported by grants from FONDAP (15090007) and ICGEB
(CRP/CHI11-01).