RGD Reference Report - Interaction between Mas1 and AT1RA contributes to enhancement of skeletal muscle angiogenesis by angiotensin-(1-7) in Dahl salt-sensitive rats. - Rat Genome Database

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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.

Authors: Exner, Eric C  Geurts, Aron M  Hoffmann, Brian R  Casati, Marc  Stodola, Timothy  Dsouza, Nikita R  Zimmermann, Michael  Lombard, Julian H  Greene, Andrew S 
Citation: Exner EC, etal., PLoS One. 2020 Apr 23;15(4):e0232067. doi: 10.1371/journal.pone.0232067. eCollection 2020.
RGD ID: 127345089
Pubmed: PMID:32324784   (View Abstract at PubMed)
PMCID: PMC7179868   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0232067   (Journal Full-text)

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.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Agtr1aRatpositive regulation of angiogenesis  IMP  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Agtr1aRatdecreased angiogenesis inducesIMP  RGD 
Agtr1aem5McwiRatdecreased angiogenesis inducesIMP  RGD 
SS-Agtr1aem5McwiRatdecreased angiogenesis inducesIMP  RGD 
Objects Annotated

Genes (Rattus norvegicus)
Agtr1a  (angiotensin II receptor, type 1a)
Agtr1aem5Mcwi  (angiotensin II receptor, type 1a; zinc finger nuclease induced mutant 5, Medical College of Wisconsin)

Strains
SS-Agtr1aem5Mcwi  (NA)


Additional Information