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Interaction between Mas1 and AT1RA contributes to enhancement of skeletal muscle angiogenesis by angiotensin-(1-7) in Dahl salt-sensitive rats.
Exner, Eric C; Geurts, Aron M; Hoffmann, Brian R; Casati, Marc; Stodola, Timothy; Dsouza, Nikita R; Zimmermann, Michael; Lombard, Julian H; Greene, Andrew S.
Afiliación
  • Exner EC; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Geurts AM; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Hoffmann BR; Genomic Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Casati M; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Stodola T; Department of Bioengineering, Medical College of Wisconsin and Marquette University, Milwaukee, Wisconsin, United States of America.
  • Dsouza NR; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Zimmermann M; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Lombard JH; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
  • Greene AS; Genomic Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
PLoS One ; 15(4): e0232067, 2020.
Article en En | MEDLINE | ID: mdl-32324784
The heptapeptide angiotensin-(1-7) (Ang-(1-7)) is protective in the cardiovascular system through its induction of vasodilator production and angiogenesis. Despite acting antagonistically to the effects of elevated, pathophysiological levels of angiotensin II (AngII), recent evidence has identified convergent and beneficial effects of low levels of both Ang-(1-7) and AngII. Previous work identified the AngII receptor type I (AT1R) as a component of the protein complex formed when Ang-(1-7) binds its receptor, Mas1. Importantly, pharmacological blockade of AT1R did not alter the effects of Ang-(1-7). Here, we use a novel mutation of AT1RA in the Dahl salt-sensitive (SS) rat to test the hypothesis that interaction between Mas1 and AT1R contributes to proangiogenic Ang-(1-7) signaling. In a model of hind limb angiogenesis induced by electrical stimulation, we find that the restoration of skeletal muscle angiogenesis in SS rats by Ang-(1-7) infusion is impaired in AT1RA knockout rats. Enhancement of endothelial cell (EC) tube formation capacity by Ang-(1-7) is similarly blunted in AT1RA mutant ECs. Transcriptional changes elicited by Ang-(1-7) in SS rat ECs are altered in AT1RA mutant ECs, and tandem mass spectrometry-based proteomics demonstrate that the protein complex formed upon binding of Ang-(1-7) to Mas1 is altered in AT1RA mutant ECs. Together, these data support the hypothesis that interaction between AT1R and Mas1 contributes to proangiogenic Ang-(1-7) signaling.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fragmentos de Péptidos / Angiotensina I / Proteínas Proto-Oncogénicas / Músculo Esquelético / Receptores Acoplados a Proteínas G / Receptor de Angiotensina Tipo 1 Tipo de estudio: Diagnostic_studies Límite: Animals Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fragmentos de Péptidos / Angiotensina I / Proteínas Proto-Oncogénicas / Músculo Esquelético / Receptores Acoplados a Proteínas G / Receptor de Angiotensina Tipo 1 Tipo de estudio: Diagnostic_studies Límite: Animals Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos