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

Ábrigo, Johanna; Simón, Felipe; Cabrera, Daniel; Cabello-Verrugio, Claudio

doi:10.1159/000452522

Cited by 33 publications

(28 citation statements)

References 63 publications

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“…Several data, mainly from our group and others, have demonstrated the anti-atrophic effect mediated by Ang-(1-7) on skeletal muscle both in vitro and in vivo [25][26][27][28][29][30][31][32]. This is the first report that shows that Ang-(1-7) inhibits myostatin-induced muscle atrophy.…”

Section: Discussionmentioning

confidence: 91%

“…We have also previously described that TGF-β, a growth factor of the same family as myostatin, induces muscle atrophy through an ROS-dependent mechanism [42]. Moreover, Ang-(1-7) decreases the TGF-β -dependent ROS production in myotubes [28]. Other studies must be performed in order to elucidate the source of ROS production by myostatin, and the mechanism through which Ang-(1-7) decreases ROS in response to myostatin.…”

Section: Discussionmentioning

confidence: 99%

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

Aravena

Ábrigo

González

et al. 2020

IJMS

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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.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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

Aravena

Ábrigo

González

et al. 2020

IJMS

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“…A previous study suggested that mesenchymal stem cell-conditioned media reduced muscle atrophy-related proteins in C2C12 cells 11,24,25 . To confirm whether hUCB-MSCs could prevent TGF-β1 induced muscle atrophy in C2C12 cell myotubes, we performed hUCB-MSCs coculture study in C2C12 cell myotubes treated with TGF-β1 and measured diameter in each group of C2C12 cell myotubes 24 hr after TGF-β1 treatment.…”

Section: Tgf-β1 Induced Muscle Atrophy Was Ameliorated By Hucb-mscsmentioning

confidence: 94%

Repeated intramuscular transplantations of hUCB-MSCs improves motor function and survival in the SOD1 G93A mice through activation of AMPK

Kook

Lee

Shin

et al. 2020

Sci Rep

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is characterized by loss of motor neurons and degeneration of neuromuscular junctions. to improve disease progression, previous studies have suggested many options that have shown beneficial effects in diseases, especially stem cell therapy. in this study, we used repeated intramuscular transplantation of human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) and observed positive effects on muscle atrophy and oxidative stress. in an in vivo study, motor function, body weight and survival rate were assessed, and skeletal muscle tissues were analyzed by western blotting and immunohistochemistry. After intramuscular transplantation, the hUcB-MScs survived within the skeletal muscle for at least 1 week. Transplantation ameliorated muscle atrophy and the rate of neuromuscular degeneration in skeletal muscle through reductions in intracellular RoS levels. Both expression of skeletal muscle atrophy markers, muscle atrophy F-box (MAFbx)/atrogin1 and muscle RING finger 1 (MuRF1), were also reduced; however, the reductions were not significant. Moreover, transplantation of hUCB-MSCs improved protein synthesis and inhibited the inoS/no signaling pathway through AMpK activation. our results suggest that repeated intramuscular transplantation of hUcB-MScs can be a practical option for stem cell therapy for ALS.

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“…ACE2, meanwhile, inactivates Ang II and is a negative regulator of Ang II-dependent signaling [39]. In this regard, ACE2/Ang-(1-7)/MasR in skeletal muscle shows anti-atrophic, anti-fibrotic, and anti-inflammatory activities [27,31,32,[61][62][63]. In murine models, this axis can increase the muscle strength and functionality of animals [64], and it can also increase the activity of Akt/mTOR-p70S6K, favoring the synthesis of muscle proteins.…”

Section: Ras and Its Role In The Loss Of Muscle Massmentioning

confidence: 99%

SARS-CoV-2/Renin–Angiotensin System: Deciphering the Clues for a Couple with Potentially Harmful Effects on Skeletal Muscle

González

Orozco-Aguilar

Achiardi

et al. 2020

IJMS

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Severe acute respiratory syndrome coronavirus (SARS-CoV-2) has produced significant health emergencies worldwide, resulting in the declaration by the World Health Organization of the coronavirus disease 2019 (COVID-19) pandemic. Acute respiratory syndrome seems to be the most common manifestation of COVID-19. A high proportion of patients require intensive care unit admission and mechanical ventilation (MV) to survive. It has been well established that angiotensin-converting enzyme type 2 (ACE2) is the primary cellular receptor for SARS-CoV-2. ACE2 belongs to the renin–angiotensin system (RAS), composed of several peptides, such as angiotensin II (Ang II) and angiotensin (1-7) (Ang-(1-7)). Both peptides regulate muscle mass and function. It has been described that SARS-CoV-2 infection, by direct and indirect mechanisms, affects a broad range of organ systems. In the skeletal muscle, through unbalanced RAS activity, SARS-CoV-2 could induce severe consequences such as loss of muscle mass, strength, and physical function, which will delay and interfere with the recovery process of patients with COVID-19. This article discusses the relationship between RAS, SARS-CoV-2, skeletal muscle, and the potentially harmful consequences for skeletal muscle in patients currently infected with and recovering from COVID-19.

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

Cited by 33 publications

References 63 publications

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

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

Repeated intramuscular transplantations of hUCB-MSCs improves motor function and survival in the SOD1 G93A mice through activation of AMPK

SARS-CoV-2/Renin–Angiotensin System: Deciphering the Clues for a Couple with Potentially Harmful Effects on Skeletal Muscle

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