adenoviral delivery of angiotensin-(1-7) or angiotensin-(1-9) inhibits cardiomyocyte hypertrophy via the mas or angiotensin type 2 receptoradenoviral交付血管紧张素-(1 - 7)或血管紧张素-(1 - 9)通过mas抑制心肌细胞肥大或血管紧张素2型受体.pdfVIP

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adenoviral delivery of angiotensin-(1-7) or angiotensin-(1-9) inhibits cardiomyocyte hypertrophy via the mas or angiotensin type 2 receptoradenoviral交付血管紧张素-(1 - 7)或血管紧张素-(1 - 9)通过mas抑制心肌细胞肥大或血管紧张素2型受体.pdf

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adenoviral delivery of angiotensin-(1-7) or angiotensin-(1-9) inhibits cardiomyocyte hypertrophy via the mas or angiotensin type 2 receptoradenoviral交付血管紧张素-(1 - 7)或血管紧张素-(1 - 9)通过mas抑制心肌细胞肥大或血管紧张素2型受体

Adenoviral Delivery of Angiotensin-(1-7) or Angiotensin- (1-9) Inhibits Cardiomyocyte Hypertrophy via the Mas or Angiotensin Type 2 Receptor ˜ ¤a ¤b ¤c ¤a Monica Flores-Munoz , Bruno M. D. C. Godinho , Abdulaziz Almalik , Stuart A. Nicklin* Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom Abstract The counter-regulatory axis of the renin angiotensin system peptide angiotensin-(1-7) [Ang-(1-7)] has been identified as a potential therapeutic target in cardiac remodelling, acting via the mas receptor. Furthermore, we recently reported that an alternative peptide, Ang-(1-9) also counteracts cardiac remodelling via the angiotensin type 2 receptor (AT2R). Here, we have engineered adenoviral vectors expressing fusion proteins which release Ang-(1-7) [RAdAng-(1-7)] or Ang-(1-9) [RAdAng-(1-9)] and compared their effects on cardiomyocyte hypertrophy in rat H9c2 cardiomyocytes or primary adult rabbit cardiomyocytes, stimulated with angiotensin II, isoproterenol or arg-vasopressin. RAdAng-(1-7) and RAdAng-(1-9) efficiently transduced cardiomyocytes, expressed fusion proteins and secreted peptides, as demonstrated by western immunoblotting and conditioned media assays. Furthermore, secreted Ang-(1-7) and Ang-(1-9) inhibited cardiomyocyte hypertrophy (Control = 168.7 68.4 m m; AngII = 232.1 610.7 m m; AngII+ RAdAng-(1-7) = 186 69.1 m m, RAdAng-(1- 9) = 180.569 mm; P,0.05) and these effects were selectively reversed by inhibitors of their cognate receptors, the mas antagonist A779 for RAdAng-(1-7) and the AT2R a