Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mas

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dc.contributor.authorMorales, M.G.
dc.contributor.authorAbrigo, J.
dc.contributor.authorAcuna, M.J.
dc.contributor.authorSantos, R.A.
dc.contributor.authorBader, M.
dc.contributor.authorBrandan, E.
dc.contributor.authorSimon, F.
dc.contributor.authorOlguin, H.
dc.contributor.authorCabrera, D.
dc.contributor.authorCabello-Verrugio, C.
dc.date.accessioned2017-08-22T20:22:24Z
dc.date.available2017-08-22T20:22:24Z
dc.date.issued2016-04
dc.descriptionIndexación: Scopus.es_CL
dc.description.abstractImmobilization is a form of disuse characterized by a loss of strength and muscle mass. Among the main features are decreased IGF-1/Akt signalling and increased ubiquitin-proteasome pathway signalling, which induce greater myosin heavy chain degradation. Activation of the classical renin-angiotensin system (RAS) causes deleterious effects in skeletal muscle, including muscle wasting. In contrast, angiotensin-(1-7) [Ang-(1-7)], a peptide of the non-classical RAS, produces beneficial effects in skeletal muscle. However, the role of Ang-(1-7) in skeletal muscle disuse atrophy and independent of classical RAS activation has not been evaluated. Therefore, we assessed the functions of Ang-(1-7) and the Mas receptor in disuse muscle atrophy in vivo using unilateral cast immobilization of the hind limb in male, 12-week-old wild-type (WT) and Mas-knockout (Mas KO) mice for 1 and 14 days. Additionally, we evaluated the participation of IGF-1/IGFR-1/Akt signalling and ubiquitin-proteasome pathway expression on the effects of Ang-(1-7) immobilization-induced muscle atrophy. Our results found that Ang-(1-7) prevented decreased muscle strength and reduced myofiber diameter, myosin heavy chain levels, and the induction of atrogin-1 and MuRF-1 expressions, all of which normally occur during immobilization. Analyses indicated that Ang-(1-7) increases IGF-1/IGFR-1/Akt pathway signalling through IGFR-1 and Akt phosphorylation, and the concomitant activation of two downstream targets of Akt, p70S6K and FoxO3. These anti-atrophic effects of Ang-(1-7) were not observed in Mas KO mice, indicating crucial participation of the Mas receptor. This report is the first to propose anti-atrophic effects of Ang-(1-7) via the Mas receptor and the participation of the IGF-1/IGFR-1/Akt/p70S6K/FoxO3 mechanism in disuse skeletal muscle atrophy.es_CL
dc.description.urihttp://dmm.biologists.org/content/9/4/441
dc.identifier.citationDisease Models & Mechanisms 2016 9: 441-449es_CL
dc.identifier.issn1754-8403
dc.identifier.issn1754-8411
dc.identifier.otherdoi: 10.1242/dmm.023390
dc.identifier.urihttp://repositorio.unab.cl/xmlui/handle/ria/3994
dc.language.isoenes_CL
dc.publisherUniversidad Andrés Belloes_CL
dc.subjectAngiotensin-(1-7)es_CL
dc.subjectAtrophyes_CL
dc.subjectDisusees_CL
dc.subjectMas receptores_CL
dc.subjectSkeletal musclees_CL
dc.titleAngiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mases_CL
dc.typeArtículoes_CL
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