Loss of melusin is a novel, neuronal NO synthase/FoxO3-independent master switch of unloading-induced muscle atrophy.

Journal of Cachexia, Sarcopenia and Muscle
Maurizio VitadelloLuisa Gorza

Abstract

Unloading/disuse induces skeletal muscle atrophy in bedridden patients and aged people, who cannot prevent it by means of exercise. Because interventions against known atrophy initiators, such as oxidative stress and neuronal NO synthase (nNOS) redistribution, are only partially effective, we investigated the involvement of melusin, a muscle-specific integrin-associated protein and a recognized regulator of protein kinases and mechanotransduction in cardiomyocytes. Muscle atrophy was induced in the rat soleus by tail suspension and in the human vastus lateralis by bed rest. Melusin expression was investigated at the protein and transcript level and after treatment of tail-suspended rats with atrophy initiator inhibitors. Myofiber size, sarcolemmal nNOS activity, FoxO3 myonuclear localization, and myofiber carbonylation of the unloaded rat soleus were studied after in vivo melusin replacement by cDNA electroporation, and muscle force, myofiber size, and atrogene expression after adeno-associated virus infection. In vivo interference of exogenous melusin with dominant-negative kinases and other atrophy attenuators (Grp94 cDNA; 7-nitroindazole) on size of unloaded rat myofibers was also explored. Unloading/disuse reduced muscle me...Continue Reading

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Citations

Apr 25, 2020·International Journal of Molecular Sciences·Violetta V KravtsovaIgor I Krivoi
Nov 21, 2020·Journal of Neuromuscular Diseases·Stefano SchiaffinoBert Blaauw
Jan 7, 2021·Cells·Luisa GorzaMara Brancaccio

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Methods Mentioned

BETA
nuclear translocation
transfection
transfections
biopsies
electrophoresis
PCR
confocal microscopy
biopsy

Software Mentioned

LabVIEW
ImageJ
SDS RQ Study
SigmaPlot

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