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dc.contributor.author
González, Germán Esteban  
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Rhaleb, N.-E.  
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D'Ambrosio, Martin A.  
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Nakagawa, Pablo  
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Liao, Tang Dong  
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Peterson, Edward L.  
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Leung, Pablo  
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Dai, Xiangguo  
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Janic, Branislava  
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Liu, Yun He  
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Yang, Xiao Ping  
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Carretero, Oscar A.  
dc.date.available
2019-10-16T20:33:20Z  
dc.date.issued
2016-11  
dc.identifier.citation
González, Germán Esteban; Rhaleb, N.-E.; D'Ambrosio, Martin A.; Nakagawa, Pablo; Liao, Tang Dong; et al.; Cardiac-deleterious role of galectin-3 in chronic Angiotensin II-induced hypertension; American Physiological Society; American Journal of Physiology - Heart and Circulatory Physiology; 311; 5; 11-2016; H1287-H1296  
dc.identifier.issn
0363-6135  
dc.identifier.uri
http://hdl.handle.net/11336/86090  
dc.description.abstract
Galectin- 3 (Gal-3), a member of the β-galactoside lectin family, has an important role in immune regulation. In hypertensive rats and heart failure patients, Gal-3 is considered a marker for an unfavorable prognosis. Nevertheless, the role and mechanism of Gal-3 action in hypertension-induced target organ damage are unknown. We hypothesized that, in angiotensin II (ANG II)-induced hypertension, genetic deletion of Gal-3 prevents left ventricular (LV) adverse remodeling and LV dysfunction by reducing the innate immune responses and myocardial fibrosis. To induce hypertension, male C57BL/6J and Gal-3 knockout (KO) mice were infused with ANG II (3 µg·min-1·kg-1 sc) for 8 wk. We assessed: 1) systolic blood pressure by plethysmography, 2) LV function and remodeling by echocardiography, 3) myocardial fibrosis by histology, 4) cardiac CD68+ macrophage infiltration by histology, 5) ICAM-1 and VCAM-1 expression by Western blotting, 6) plasma cytokines, including interleukin- 6 (IL-6), by enzyme-linked immunosorbent assay, and 7) regulatory T (Treg) cells by flow cytometry as detected by their combined expression of CD4, CD25, and FOXP3. Systolic blood pressure and cardiac hypertrophy increased similarly in both mouse strains when infused with ANG II. However, hypertensive C57BL/6J mice suffered impaired ejection and shortening fractions. In these mice, the extent of myocardial fibrosis and macrophage infiltration was greater in histological sections, and cardiac ICAM-1, as well as plasma IL-6, expression was higher as assessed by Western blotting. However, all these parameters were blunted in Gal-3 KO mice. Hypertensive Gal-3 KO mice also had a higher number of splenic Treg lymphocytes. In conclusion, in ANG II-induced hypertension, genetic deletion of Gal-3 prevented LV dysfunction without affecting blood pressure or LV hypertrophy. This study indicates that the ANG II effects are, in part, mediated or triggered by Gal-3 together with the related intercellular signaling (ICAM-1 and IL-6), leading to cardiac inflammation and fibrosis.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
American Physiological Society  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
ANGIOTENSIN II  
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FIBROSIS  
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GALECTIN-3  
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HYPERTENSION  
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INFLAMMATION  
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INTERLEUKIN-6  
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MACROPHAGES  
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Patología  
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Medicina Básica  
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CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
Cardiac-deleterious role of galectin-3 in chronic Angiotensin II-induced hypertension  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
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info:eu-repo/semantics/publishedVersion  
dc.date.updated
2019-08-30T13:56:38Z  
dc.journal.volume
311  
dc.journal.number
5  
dc.journal.pagination
H1287-H1296  
dc.journal.pais
Estados Unidos  
dc.journal.ciudad
Bethesda  
dc.description.fil
Fil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Henry Ford Hospital; Estados Unidos  
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Fil: Rhaleb, N.-E.. Henry Ford Hospital; Estados Unidos. Wayne State University; Estados Unidos  
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Fil: D'Ambrosio, Martin A.. Henry Ford Hospital; Estados Unidos  
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Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados Unidos  
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Fil: Liao, Tang Dong. Henry Ford Hospital; Estados Unidos  
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Fil: Peterson, Edward L.. Henry Ford Hospital; Estados Unidos  
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Fil: Leung, Pablo. Henry Ford Hospital; Estados Unidos  
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Fil: Dai, Xiangguo. Henry Ford Hospital; Estados Unidos  
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Fil: Janic, Branislava. Henry Ford Hospital; Estados Unidos  
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Fil: Liu, Yun He. Henry Ford Hospital; Estados Unidos  
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Fil: Yang, Xiao Ping. Henry Ford Hospital; Estados Unidos  
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Fil: Carretero, Oscar A.. Henry Ford Hospital; Estados Unidos  
dc.journal.title
American Journal of Physiology - Heart and Circulatory Physiology  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/ajpheart.00096.2016  
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info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5130499/  
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info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/full/10.1152/ajpheart.00096.2016?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed