Angiotensin-(1–7) decreases skeletal muscle atrophy induced by angiotensin II through a Mas receptor-dependent mechanism

2014 ◽  
Vol 128 (5) ◽  
pp. 307-319 ◽  
Author(s):  
Franco Cisternas ◽  
María Gabriela Morales ◽  
Carla Meneses ◽  
Felipe Simon ◽  
Enrique Brandan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Angiotensin Ii ◽  
Muscle Atrophy ◽  
Membrane Receptor ◽  
Skeletal Muscle Atrophy ◽  
Akt Phosphorylation ◽  
Mas Receptor ◽  
Plasma Membrane Receptor ◽  
Dependent Mechanism

Angiotensin-(1–7) produces an anti-atrophic effect in our model of skeletal muscle atrophy induced by angiotensin II, which is mediated by its plasma membrane receptor Mas. Angiotensin-(1–7) exerts its anti-atrophic effects, at least, by inducing AKT phosphorylation.

scholarly journals Deletion of NAD(P)H Oxidase 2 Prevents Angiotensin II-Induced Skeletal Muscle Atrophy

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Tomoyasu Kadoguchi ◽  
Shingo Takada ◽  
Takashi Yokota ◽  
Takaaki Furihata ◽  
Junichi Matsumoto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Angiotensin Ii ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Muscle Weight ◽  
Cross Sectional ◽  
Akt Phosphorylation ◽  
Protein Synthesis And Degradation ◽  
Synthesis And Degradation

Skeletal muscle atrophy is induced by an imbalance between protein synthesis and degradation. Our previous studies reported that angiotensin II (AII) directly induced muscle atrophy in mice. This study investigated the role of NAD(P)H oxidase 2 (Nox2) activation by AII in the induction of skeletal muscle atrophy. For 4 weeks, either saline (vehicle: V) or AII (1000 ng kg−1 min−1) was infused into male wild-type (WT) and Nox2 knockout (KO) mice via osmotic minipumps. Experiments were performed in the following 4 groups: WT + V, KO + V, WT + AII, and KO + AII. Body weight, muscle weight, and myocyte cross-sectional area were significantly decreased in WT + AII compared to WT + V mice, and these changes were not observed in KO + AII mice. Akt phosphorylation of Ser473 and p70S6K of Thr389 was decreased, gene expression levels of MuRF-1 and atrogin-1 were increased in WT + AII compared to WT + V, and these changes were significantly attenuated in KO + AII mice. The deletion of Nox2 prevented AII-induced skeletal muscle atrophy via improving the balance between protein synthesis and degradation. Therefore, Nox2 may be a therapeutic target for AII-induced skeletal muscle atrophy.

scholarly journals Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy

2020 ◽  
Vol 21 (3) ◽  
pp. 1167 ◽  
Author(s):  
Javier Aravena ◽  
Johanna Abrigo ◽  
Francisco Gonzalez ◽  
Francisco Aguirre ◽  
Andrea Gonzalez ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Renin Angiotensin System ◽  
Ubiquitin Proteasome System ◽  
Skeletal Muscle Atrophy ◽  
Gene Expressions ◽  
Protein Levels ◽  
Mas Receptor ◽  
Signaling Activation ◽  
Species Production

Myostatin is a myokine that regulates muscle function and mass, producing muscle atrophy. Myostatin induces the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. The main pathway that mediates protein degradation during muscle atrophy is the ubiquitin proteasome system, by increasing the expression of atrogin-1 and MuRF-1. In addition, myostatin activates the NF-κB signaling pathway. Renin–angiotensin system (RAS) also regulates muscle mass. Angiotensin (1-7) (Ang-(1-7)) has anti-atrophic properties in skeletal muscle. In this paper, we evaluated the effect of Ang-(1-7) on muscle atrophy and signaling induced by myostatin. The results show that Ang-(1-7) prevented the decrease of the myotube diameter and myofibrillar protein levels induced by myostatin. Ang-(1-7) also abolished the increase of myostatin-induced reactive oxygen species production, atrogin-1, MuRF-1, and TNF-α gene expressions and NF-κB signaling activation. Ang-(1-7) inhibited the activity mediated by myostatin through Mas receptor, as is demonstrated by the loss of all Ang-(1-7)-induced effects when the Mas receptor antagonist A779 was used. Our results show that the effects of Ang-(1-7) on the myostatin-dependent muscle atrophy and signaling are blocked by MK-2206, an inhibitor of Akt/PKB. Together, these data indicate that Ang-(1-7) inhibited muscle atrophy and signaling induced by myostatin through a mechanism dependent on Mas receptor and Akt/PKB.

Sirtuin 3 deficiency accelerates Angiotensin II-induced skeletal muscle atrophy

2019 ◽  
Vol 61 (6) ◽  
pp. 586-593
Author(s):  
Jianheng Zheng ◽  
Jing Gao ◽  
Qiuping Zhang ◽  
Xiahong Wu ◽  
Weili Shen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Sirtuin 3

scholarly journals Angiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth Factor Type Beta (TGF-β) via Mas Receptor Activation

2016 ◽  
Vol 40 (1-2) ◽  
pp. 27-38 ◽  
Author(s):  
Johanna Ábrigo ◽  
Felipe Simon ◽  
Daniel Cabrera ◽  
Claudio Cabello-Verrugio
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Western Blot ◽  
Muscle Atrophy ◽  
Transforming Growth Factor ◽  
Fibre Diameter ◽  
Skeletal Muscle Atrophy ◽  
Mas Receptor ◽  
Factor Type ◽  
Tgf Β1

Background: Transforming growth factor type beta 1 (TGF-β1) produces skeletal muscle atrophy. Angiotensin-(1-7) (Ang-(1-7)), through the Mas receptor, prevents the skeletal muscle atrophy induced by sepsis, immobilization, or angiotensin II (Ang-II). However, the effect of Ang-(1-7) on muscle wasting induced by TGF-β1 is unknown. Aim: To evaluate whether Ang-(1-7)/Mas receptor axis could prevent the skeletal muscle atrophy induced by TGF-β1. Methods: This study assessed the atrophic effect of TGF-β1 in C2C12 myotubes and mice in absence or presence of Ang-(1-7), and the receptor participation using A779, an antagonist of the Mas receptor. The levels of myosin heavy chain (MHC), polyubiquitination, and MuRF-1 were detected by western blot. Myotube diameter was also evaluated. In vivo analysis included the muscle strength, fibre diameter, MHC and MuRF-1 levels by western blot, and ROS levels by DCF probe detection. Results: The results showed that Ang-(1-7) prevented the increase in MuRF-1 and polyubiquitined protein levels, the decrease of MHC levels, the myotubes/fibre diameter diminution, and the increased production of reactive oxygen species (ROS) induced by TGF-β1. Utilizing A779 inhibited the anti-atrophic effect of Ang-(1-7). Conclusion: The preventive effect of Ang-(1-7) on skeletal muscle atrophy induced by TGF-β1 is produced through inhibition of ROS production and proteasomal degradation of MHC.

Angiotensin II: Role in Skeletal Muscle Atrophy

2012 ◽  
Vol 13 (6) ◽  
pp. 560-569 ◽  
Author(s):  
Claudio Cabello-Verrugio ◽  
Gonzalo Cordova ◽  
Jose Diego Salas
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy

scholarly journals Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression

2015 ◽  
Vol 117 (5) ◽  
pp. 424-436 ◽  
Author(s):  
Philipp Du Bois ◽  
Cristina Pablo Tortola ◽  
Doerte Lodka ◽  
Melanie Kny ◽  
Franziska Schmidt ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy

The angiotensin-(1–7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice

2014 ◽  
Vol 467 (9) ◽  
pp. 1975-1984 ◽  
Author(s):  
Carla Meneses ◽  
María Gabriela Morales ◽  
Johanna Abrigo ◽  
Felipe Simon ◽  
Enrique Brandan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy

scholarly journals The Molecular Mechanisms of Calpains Action on Skeletal Muscle Atrophy

2016 ◽  
pp. 547-560 ◽  
Author(s):  
J. HUANG ◽  
X. ZHU
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Therapeutic Interventions ◽  
Skeletal Muscle Atrophy ◽  
Akt Phosphorylation ◽  
Downstream Effects ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway

Skeletal muscle atrophy is associated with a loss of muscle protein which may result from both increased proteolysis and decreased protein synthesis. Investigations on cell signaling pathways that regulate muscle atrophy have promoted our understanding of this complicated process. Emerging evidence implicates that calpains play key roles in dysregulation of proteolysis seen in muscle atrophy. Moreover, studies have also shown that abnormally activated calpain results muscle atrophy via its downstream effects on ubiquitin-proteasome pathway (UPP) and Akt phosphorylation. This review will discuss the role of calpains in regulation of skeletal muscle atrophy mainly focusing on its collaboration with either UPP or Akt in atrophy conditions in hope to stimulate the interest in development of novel therapeutic interventions for skeletal muscle atrophy.

scholarly journals Angiotensin-(1-7) Prevents Lipopolysaccharide-Induced Autophagy via the Mas Receptor in Skeletal Muscle

2020 ◽  
Vol 21 (24) ◽  
pp. 9344
Author(s):  
Juan Carlos Rivera ◽  
Johanna Abrigo ◽  
Franco Tacchi ◽  
Felipe Simon ◽  
Enrique Brandan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
B Cell Lymphoma ◽  
Mapk Signaling ◽  
C2c12 Cells ◽  
Skeletal Muscle Atrophy ◽  
Autophagic Flux ◽  
Mrna Levels ◽  
Mas Receptor ◽  
The Impact

Skeletal muscle atrophy, which occurs in lipopolysaccharide (LPS)-induced sepsis, causes a severe muscle function reduction. The increased autophagy contributes to sepsis-induced skeletal muscle atrophy in a model of LPS injection, increasing LC3II/LC3I ratio, autophagy flux, and autophagosomes. Angiotensin-(1-7) (Ang-(1-7)) has anti-atrophic effects via the Mas receptor in skeletal muscle. However, the impact of Ang-(1-7) on LPS-induced autophagy is unknown. In this study, we determined the effect of Ang-(1-7) on sepsis-induced muscle autophagy. C57BL6 wild-type (WT) mice and mice lacking the Mas receptor (KO Mas) were injected with LPS together with the systemic administration of Ang-(1-7) to determine autophagy in skeletal muscle. We also evaluated autophagy and p38 and c-Jun N-terminal kinase (JNK)activation. Our results show that Ang-(1-7) prevents LPS-induced autophagy in the diaphragm, tibialis anterior, and gastrocnemius of WT mice, which is demonstrated by a decrease in the LC3II/LC3I ratio and mRNA levels of lc3b and ctsl. This effect was lost in KO Mas mice, suggesting the role of the Mas receptor. The results in C2C12 cells show that Ang-(1-7) reduces several LPS-dependent effects, such as autophagy (LC3II/LC3I ratio, autophagic flux, and autophagosomes), activation of p38 and JNK, B-cell lymphoma-2 (BCL2) phosphorylation, and disassembly of the Beclin1/BCL2 complex. In conclusion, Ang-(1-7)/Mas receptor reduces LPS-induced autophagy in skeletal muscle. In vitro assays indicate that Ang-(1-7) prevents LPS-induced autophagy and modifies the MAPK signaling and the disassembly of a complex involved at the beginning of autophagy.

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1–7) through a p38 MAPK-dependent mechanism

2015 ◽  
Vol 129 (6) ◽  
pp. 461-476 ◽  
Author(s):  
María Gabriela Morales ◽  
Hugo Olguín ◽  
Gabriella Di Capua ◽  
Enrique Brandan ◽  
Felipe Simon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
P38 Mapk ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Skeletal Muscle Wasting ◽  
Catabolic Response ◽  
Dependent Mechanism

In this study we determined that angiotensin-(1–7) is a novel peptide that prevents the skeletal muscle atrophy observed in a model of sepsis by inhibiting the catabolic response developed in skeletal muscle and improving its performance.

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