dc.creatorSepúlveda, Francisco
dc.creatorSaavedra, Eduardo
dc.creatorSánchez, Rodrigo
dc.creatorCórdova, Sebastián
dc.creatorLemus, David
dc.creatorFuenzalida, Marcela
dc.creatorVergara, Marcela
dc.creatorRosas, Carlos
dc.date.accessioned2020-11-03T07:49:21Z
dc.date.accessioned2023-05-30T20:46:08Z
dc.date.available2020-11-03T07:49:21Z
dc.date.available2023-05-30T20:46:08Z
dc.date.created2020-11-03T07:49:21Z
dc.date.issued2019
dc.identifier0717-9502
dc.identifierhttp://dspace-uss.eastus.cloudapp.azure.com:8080/xmlui/handle/uss/329
dc.identifierhttp://dx.doi.org/10.4067/S0717-95022019000100048
dc.identifier0717-9367
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/6446569
dc.description.abstractThe VEGF levels and its binding to its receptors are key stages in the regulation of angiogenesis. Acetylsalicylic acid (ASA), widely used in post-myocardial infarction treatment, has been shown to have an anti-angiogenic effect in tumor models. This potentially counterproductive effect requires to be studied in myocardium. The aim of this study is to quantify the effect of ASA and salicylic acid (SA) on the vascularization in chick allantochorionic membrane (CAM) and on the levels of VEGF-A and VEGFR2 in myocardium of chicken embryos. Thirty White Leghorn chicken fetuses were instilled at 10 days of gestation with 60 mL of 0.1 % DMSO (control) or also containing 0.3 mmol of ASA or SA. After 48 hours, CAM histological processing was performed to count blood vessels and heart tissue to quantify VEGF-A and VEGFR2 by immunohistochemistry. Immunoreactivity was quantified by Image J. Both ASA and SA decreased CAM microvascular density. In myocardium, AAS, although not SA, decreased the concentration of VEGFR2. There was no effect on VEGF-A. In our experimental model, chicken fetuses at 10 days of gestation, the inhibitory effect of ASA on angiogenesis in CAM were also observed. The decrease in VEGFR2 in cardiomyocytes suggests that ASA also affects angiogenesis in healthy myocardium, modifying the availability of the receptor to VEGF. These findings allow us to postulate that ASA could interfere with tissue regeneration, when it is required, as post myocardial infarction.
dc.languagespa
dc.publisherFacultad de Medicina y Ciencia
dc.relationvol. 37, no. 1, p. 48-53
dc.relationIndexado en WOS
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile
dc.sourceInternational Journal of Morphology
dc.subjectASPIRIN
dc.subjectHEART
dc.subjectVEGF RECEPTOR
dc.subjectANGIOGENESIS
dc.subjectASPIRINA
dc.subjectCORAZÓN
dc.subjectRECEPTOR DE VEGF
dc.subjectENDOTHELIAL GROWTH-FACTOR
dc.subjectINHIBITION
dc.titleExpresión de VEGF-A y VEGFR2 en Miocardio de Pollos Tratados con Ácido Acetilsalicílico (AAS)
dc.typeArticle


Este ítem pertenece a la siguiente institución