PMID- 27842312
OWN - NLM
STAT- MEDLINE
DCOM- 20170213
LR  - 20211203
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 40
IP  - 1-2
DP  - 2016
TI  - Angiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth 
      Factor Type Beta (TGF-beta) via Mas Receptor Activation.
PG  - 27-38
AB  - BACKGROUND: Transforming growth factor type beta 1 (TGF-beta1) 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-beta1 is 
      unknown. AIM: To evaluate whether Ang-(1-7)/Mas receptor axis could prevent the 
      skeletal muscle atrophy induced by TGF-beta1. METHODS: This study assessed the 
      atrophic effect of TGF-beta1 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-beta1. 
      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-beta1 is 
      produced through inhibition of ROS production and proteasomal degradation of MHC.
CI  - (c) 2016 The Author(s) Published by S. Karger AG, Basel.
FAU - Abrigo, Johanna
AU  - Abrigo J
AD  - Departmento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad 
      de Medicina, Universidad Andres Bello, Santiago, Chile.
FAU - Simon, Felipe
AU  - Simon F
FAU - Cabrera, Daniel
AU  - Cabrera D
FAU - Cabello-Verrugio, Claudio
AU  - Cabello-Verrugio C
LA  - eng
PT  - Journal Article
DEP - 20161114
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Muscle Proteins)
RN  - 0 (Peptide Fragments)
RN  - 0 (Proto-Oncogene Mas)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tripartite Motif Proteins)
RN  - 0 (Ubiquitin)
RN  - 120904-94-1 (Polyubiquitin)
RN  - 9041-90-1 (Angiotensin I)
RN  - EC 2.3.2.27 (Trim63 protein, mouse)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
RN  - EC 3.6.4.1 (Myosin Heavy Chains)
RN  - EC 3.6.4.1 (Myosins)
RN  - IJ3FUK8MOF (angiotensin I (1-7))
SB  - IM
MH  - Angiotensin I/*therapeutic use
MH  - Animals
MH  - Cell Line
MH  - Mice, Inbred C57BL
MH  - Muscle Fibers, Skeletal/drug effects/metabolism/pathology
MH  - Muscle Proteins/metabolism
MH  - Muscle, Skeletal
MH  - Muscular Atrophy/*drug therapy/pathology
MH  - Myosin Heavy Chains/metabolism
MH  - Myosins/metabolism
MH  - Peptide Fragments/*therapeutic use
MH  - Polyubiquitin/metabolism
MH  - Proteasome Endopeptidase Complex/metabolism
MH  - Proto-Oncogene Mas
MH  - Proto-Oncogene Proteins/*metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, G-Protein-Coupled/*metabolism
MH  - Transforming Growth Factor beta/*metabolism/pharmacology
MH  - Tripartite Motif Proteins/metabolism
MH  - Ubiquitin/metabolism
MH  - Ubiquitin-Protein Ligases/metabolism
MH  - Ubiquitination/drug effects
EDAT- 2016/11/15 06:00
MHDA- 2017/02/14 06:00
CRDT- 2016/11/15 06:00
PHST- 2016/09/01 00:00 [accepted]
PHST- 2016/11/15 06:00 [pubmed]
PHST- 2017/02/14 06:00 [medline]
PHST- 2016/11/15 06:00 [entrez]
AID - 000452522 [pii]
AID - 10.1159/000452522 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2016;40(1-2):27-38. doi: 10.1159/000452522. Epub 2016 Nov 
      14.