Angiotensin (1-7) counteracts the negative effect of angiotensin II on insulin signalling in HUVECs.

@article{Tassone2013AngiotensinC,
  title={Angiotensin (1-7) counteracts the negative effect of angiotensin II on insulin signalling in HUVECs.},
  author={Eliezer Joseph Tassone and Angela Sciacqua and Francesco Andreozzi and Ivan Presta and Maria Perticone and Daniela Carnevale and Manuel Casaburo and Marta Letizia Hribal and Giorgio Sesti and Francesco Perticone},
  journal={Cardiovascular research},
  year={2013},
  volume={99 1},
  pages={
          129-36
        }
}
AIMS Angiotensin II participates to the regulation of cardiovascular physiology and it is involved in molecular mechanisms of insulin resistance. Angiotensin (1-7), derived from angiotensin II metabolism, is able to counteract many of the haemodynamic and non-haemodynamic actions of angiotensin II. In this study, we investigated in human umbilical vein endothelial cells (HUVECs) the possible action of angiotensin (1-7) on the insulin signalling pathway. METHODS AND RESULTS We stimulated… 
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Angiotensin-converting enzyme 2 and angiotensin 1–7: novel therapeutic targets
TLDR
The ACE2-mediated catabolism of angiotensin II is likely to have a major role in cardiovascular protection, whereas the relevant functions and signalling mechanisms of actions induced by ang Elliotensin 1–7 have not been conclusively determined.
The Ang-(1-7)/Mas-1 axis attenuates the expression and signalling of TGF-β1 induced by AngII in mouse skeletal muscle.
TLDR
The hypothesis that Ang-(1-7) decreases the expression and further biological activity of TGF-β1 induced by AngII in–vitro and in vivo is supported.
Effects of Ang 1-7 and Endothelial Microvesicles on Ang II-induced Dysfunction and Apoptosis in Cerebral Endothelial Cells
TLDR
It is found that Ang II dose-dependently induced HbmEC apoptosis and that both Ang 1-7 and EMVs can counteract the effects of Ang II, and their protective effects were associated with ROS/NO production which were linked to Nox2, and Akt /eNOS pathways.
Nonclassical Axis of the Renin-Angiotensin System and Neprilysin: Key Mediators That Underlie the Cardioprotective Effect of PPAR-Alpha Activation during Myocardial Ischemia in a Metabolic Syndrome Model
TLDR
The regulation of the nonclassical axis of RAS forms part of a novel protective effect of fenofibrate in myocardial ischemia, and PPAR-alpha activation by fen ofibrate reverts some of the effects caused by these pathologies.
Modulation of the action of insulin by angiotensin-(1-7).
TLDR
It is demonstrated that Ang-(1-7) improves the action of insulin and opposes the negative effect that AngII exerts at this level, and potential therapeutic approaches leading to modulation of the ACE2 (angiotensin-converting enzyme 2)/Ang-( 1-7)/Mas receptor axis as a very attractive strategy in the therapy of the metabolic syndrome and diabetes-associated diseases are discussed.
Heat Shock Prevents Insulin Resistance–Induced Vascular Complications by Augmenting Angiotensin-(1-7) Signaling
TLDR
It is reported here for the first time that insulin resistance inhibits vascular HS protein (HSP) 72 expression and proposed that induction of HSP72 is a novel approach to prevent insulin resistance–induced vascular complications.
Roles of I2PP2A in the downregulation of eNOS Ser1177 phosphorylation by angiotensin II-activated PP2A.
Ginsenoside Rc Ameliorates Endothelial Insulin Resistance via Upregulation of Angiotensin-Converting Enzyme 2
TLDR
It is demonstrated that ginsenoside Rc ameliorated endothelial IR and endothelial dysfunction, at least in part, via upregulation of ACE2 and holds promise for the treatment of diabetic vascular complications.
24 h pre-incubation of EA . hy 926 cells with angiotensin II regulates insulin-dependent activation of eNOS in a concentration-dependent manner
TLDR
Angiotensin II concentrationdependently regulated basal and insulin-mediated PI3Kinase-AKT-eNOS signalling in cultured endothelial cells and showed significant attenuated insulin induced phosphorylation of eNOS Ser-1177 and AKT Ser-473, alongside impaired NOS activity.
Angiotensin II Decreases Endothelial Nitric Oxide Synthase Phosphorylation via AT1R Nox/ROS/PP2A Pathway
TLDR
Results indicated that AngII/AT1R pathway activated PP2A by downregulating its catalytic subunit Tyr307 phosphorylation, which relies on the Nox activation and ROS production.
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