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The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice
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The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice
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Journal Article
The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice
2017
Overview
Angiotensin (1-7) (Ang-(1-7)) is a bioactive heptapeptide with a short half-life and has beneficial effects in several tissues - among them, skeletal muscle - by preventing muscle atrophy. Dendrimers are promising vehicles for the protection and transport of numerous bioactive molecules. This work explored the use of a neutral, non-cytotoxic hydroxyl-terminated poly(amidoamine) (PAMAM-OH) dendrimer as an Ang-(1-7) carrier. Bioinformatics analysis showed that the Ang-(1-7)-binding capacity of the dendrimer presented a 2:1 molar ratio. Molecular dynamics simulation analysis revealed the capacity of neutral PAMAM-OH to protect Ang-(1-7) and form stable complexes. The peptide coverage ability of the dendrimer was between ~50% and 65%. Furthermore, an electrophoretic mobility shift assay demonstrated that neutral PAMAM-OH effectively bonded peptides. Experimental results showed that the Ang-(1-7)/PAMAM-OH complex, but not Ang-(1-7) alone, had an anti-atrophic effect when administered intraperitoneally, as evaluated by muscle strength, fiber diameter, myofibrillar protein levels, and atrogin-1 and MuRF-1 expressions. The results of the Ang-(1-7)/PAMAM-OH complex being intraperitoneally injected were similar to the results obtained when Ang-(1-7) was systemically administered through mini-osmotic pumps. Together, the results suggest that Ang-(1-7) can be protected for PAMAM-OH when this complex is intraperitoneally injected. Therefore, the Ang-(1-7)/PAMAM-OH complex is an efficient delivery method for Ang-(1-7), since it improves the anti-atrophic activity of this peptide in skeletal muscle.
Publisher
Dove Medical Press Limited,Dove Medical Press
Subject
/ Angiotensin I - pharmacology
/ Angiotensin I - therapeutic use
/ Animals
/ atrophy
/ carrier
/ dendrimer-peptide interactions
/ Electrophoretic Mobility Shift Assay
/ Male
/ Molecular Dynamics Simulation
/ Muscle Proteins - metabolism
/ Muscle, Skeletal - drug effects
/ Muscle, Skeletal - pathology
/ Muscular Atrophy - drug therapy
/ Muscular Atrophy - prevention & control
/ Muscular Disorders, Atrophic - drug therapy
/ Muscular Disorders, Atrophic - pathology
/ Muscular Disorders, Atrophic - prevention & control
/ Myosin Heavy Chains - metabolism
/ Peptide Fragments - pharmacology
/ Peptide Fragments - therapeutic use
/ SKP Cullin F-Box Protein Ligases - metabolism
