Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome

Autores
García, Rodrigo Damián; Ramirez, Jesica Magalí; Peral de Bruno, María; Miatello, Roberto Miguel; Renna, Nicolas Federico
Año de publicación
2019
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
To demonstrate that LZC696 (L) reduces organ damage in an experimental model of metabolic syndrome, were explored two mechanisms: anti-inflammatory effects through the IL-6Ralpha pathway and through MAS1R, the production of endothelial repair mediated by VEGFR2+/CD133+ endothelial progenitor cells (EPCs). Experimental model of metabolic syndrome was realized by WKY rats and SHRs. SHR and WKY received a fructose diet in drinking water at 10% v/v for 12 weeks (FFHR and FFR receptivity). Chronic treatment with L: (68 mg / kg per day for 6 weeks) and valsartan (V) (34 mg / kg per day for 6 weeks, as control equimolar group. Was determined: SBP, fast glycaemia and TTGO, left ventricular hypertrophy (HVI), vascular remodelling, hsCPR expression, and vascular expression in mesenteric tissue of IL-6Ralfa, STAT3, VEGFR2 and CD133 were determined. The experimental model was confirmed. L treatment reverted SBP, HVI, remodelling and vascular inflammation, decreased STAT3 expression and hsCPR in FFHR. Additionally, the most important finding was that L produced an increase in the expression of resident EPCs in the endothelial tissue of mesenteric tissue.
Fil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Ramirez, Jesica Magalí. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Genetica; Argentina
Fil: Peral de Bruno, María. Universidad Nacional de Tucumán. Facultad de Medicina; Argentina
Fil: Miatello, Roberto Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Renna, Nicolas Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Materia
remodelado vascular
inflamación vascular
LCZ696
vía IL-6R
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/124238

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network_name_str CONICET Digital (CONICET)
spelling Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndromeGarcía, Rodrigo DamiánRamirez, Jesica MagalíPeral de Bruno, MaríaMiatello, Roberto MiguelRenna, Nicolas Federicoremodelado vascularinflamación vascularLCZ696vía IL-6Rhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3To demonstrate that LZC696 (L) reduces organ damage in an experimental model of metabolic syndrome, were explored two mechanisms: anti-inflammatory effects through the IL-6Ralpha pathway and through MAS1R, the production of endothelial repair mediated by VEGFR2+/CD133+ endothelial progenitor cells (EPCs). Experimental model of metabolic syndrome was realized by WKY rats and SHRs. SHR and WKY received a fructose diet in drinking water at 10% v/v for 12 weeks (FFHR and FFR receptivity). Chronic treatment with L: (68 mg / kg per day for 6 weeks) and valsartan (V) (34 mg / kg per day for 6 weeks, as control equimolar group. Was determined: SBP, fast glycaemia and TTGO, left ventricular hypertrophy (HVI), vascular remodelling, hsCPR expression, and vascular expression in mesenteric tissue of IL-6Ralfa, STAT3, VEGFR2 and CD133 were determined. The experimental model was confirmed. L treatment reverted SBP, HVI, remodelling and vascular inflammation, decreased STAT3 expression and hsCPR in FFHR. Additionally, the most important finding was that L produced an increase in the expression of resident EPCs in the endothelial tissue of mesenteric tissue.Fil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Ramirez, Jesica Magalí. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Genetica; ArgentinaFil: Peral de Bruno, María. Universidad Nacional de Tucumán. Facultad de Medicina; ArgentinaFil: Miatello, Roberto Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Renna, Nicolas Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaOpen Access Text2019-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/124238García, Rodrigo Damián; Ramirez, Jesica Magalí; Peral de Bruno, María; Miatello, Roberto Miguel; Renna, Nicolas Federico; Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome; Open Access Text; Trends in Research; 2; 4; 2-2019; 1-62516-7138CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.oatext.com/dual-arb-nep-inhibition-improved-endothelial-function-in-metabolic-syndrome.php#gsc.tab=0info:eu-repo/semantics/altIdentifier/doi/10.15761/TR.1000143info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:31:49Zoai:ri.conicet.gov.ar:11336/124238instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:31:49.319CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
title Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
spellingShingle Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
García, Rodrigo Damián
remodelado vascular
inflamación vascular
LCZ696
vía IL-6R
title_short Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
title_full Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
title_fullStr Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
title_full_unstemmed Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
title_sort Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome
dc.creator.none.fl_str_mv García, Rodrigo Damián
Ramirez, Jesica Magalí
Peral de Bruno, María
Miatello, Roberto Miguel
Renna, Nicolas Federico
author García, Rodrigo Damián
author_facet García, Rodrigo Damián
Ramirez, Jesica Magalí
Peral de Bruno, María
Miatello, Roberto Miguel
Renna, Nicolas Federico
author_role author
author2 Ramirez, Jesica Magalí
Peral de Bruno, María
Miatello, Roberto Miguel
Renna, Nicolas Federico
author2_role author
author
author
author
dc.subject.none.fl_str_mv remodelado vascular
inflamación vascular
LCZ696
vía IL-6R
topic remodelado vascular
inflamación vascular
LCZ696
vía IL-6R
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv To demonstrate that LZC696 (L) reduces organ damage in an experimental model of metabolic syndrome, were explored two mechanisms: anti-inflammatory effects through the IL-6Ralpha pathway and through MAS1R, the production of endothelial repair mediated by VEGFR2+/CD133+ endothelial progenitor cells (EPCs). Experimental model of metabolic syndrome was realized by WKY rats and SHRs. SHR and WKY received a fructose diet in drinking water at 10% v/v for 12 weeks (FFHR and FFR receptivity). Chronic treatment with L: (68 mg / kg per day for 6 weeks) and valsartan (V) (34 mg / kg per day for 6 weeks, as control equimolar group. Was determined: SBP, fast glycaemia and TTGO, left ventricular hypertrophy (HVI), vascular remodelling, hsCPR expression, and vascular expression in mesenteric tissue of IL-6Ralfa, STAT3, VEGFR2 and CD133 were determined. The experimental model was confirmed. L treatment reverted SBP, HVI, remodelling and vascular inflammation, decreased STAT3 expression and hsCPR in FFHR. Additionally, the most important finding was that L produced an increase in the expression of resident EPCs in the endothelial tissue of mesenteric tissue.
Fil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Ramirez, Jesica Magalí. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Genetica; Argentina
Fil: Peral de Bruno, María. Universidad Nacional de Tucumán. Facultad de Medicina; Argentina
Fil: Miatello, Roberto Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Renna, Nicolas Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
description To demonstrate that LZC696 (L) reduces organ damage in an experimental model of metabolic syndrome, were explored two mechanisms: anti-inflammatory effects through the IL-6Ralpha pathway and through MAS1R, the production of endothelial repair mediated by VEGFR2+/CD133+ endothelial progenitor cells (EPCs). Experimental model of metabolic syndrome was realized by WKY rats and SHRs. SHR and WKY received a fructose diet in drinking water at 10% v/v for 12 weeks (FFHR and FFR receptivity). Chronic treatment with L: (68 mg / kg per day for 6 weeks) and valsartan (V) (34 mg / kg per day for 6 weeks, as control equimolar group. Was determined: SBP, fast glycaemia and TTGO, left ventricular hypertrophy (HVI), vascular remodelling, hsCPR expression, and vascular expression in mesenteric tissue of IL-6Ralfa, STAT3, VEGFR2 and CD133 were determined. The experimental model was confirmed. L treatment reverted SBP, HVI, remodelling and vascular inflammation, decreased STAT3 expression and hsCPR in FFHR. Additionally, the most important finding was that L produced an increase in the expression of resident EPCs in the endothelial tissue of mesenteric tissue.
publishDate 2019
dc.date.none.fl_str_mv 2019-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/124238
García, Rodrigo Damián; Ramirez, Jesica Magalí; Peral de Bruno, María; Miatello, Roberto Miguel; Renna, Nicolas Federico; Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome; Open Access Text; Trends in Research; 2; 4; 2-2019; 1-6
2516-7138
CONICET Digital
CONICET
url http://hdl.handle.net/11336/124238
identifier_str_mv García, Rodrigo Damián; Ramirez, Jesica Magalí; Peral de Bruno, María; Miatello, Roberto Miguel; Renna, Nicolas Federico; Dual ARB/NEP Inhibition with LCZ696 improved endothelial regeneration in an experimental model of metabolic syndrome; Open Access Text; Trends in Research; 2; 4; 2-2019; 1-6
2516-7138
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.oatext.com/dual-arb-nep-inhibition-improved-endothelial-function-in-metabolic-syndrome.php#gsc.tab=0
info:eu-repo/semantics/altIdentifier/doi/10.15761/TR.1000143
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Open Access Text
publisher.none.fl_str_mv Open Access Text
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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