Next Article in Journal
Actin and Myosin in Non-Neuronal Exocytosis
Next Article in Special Issue
Extracellular Vesicles from Skeletal Muscle Cells Efficiently Promote Myogenesis in Induced Pluripotent Stem Cells
Previous Article in Journal
Veterinary Regenerative Medicine for Musculoskeletal Disorders: Can Mesenchymal Stem/Stromal Cells and Their Secretome Be the New Frontier?
Previous Article in Special Issue
The Survey of Cells Responsible for Heterotopic Ossification Development in Skeletal Muscles—Human and Mouse Models
Open AccessArticle

Parkin Overexpression Attenuates Sepsis-Induced Muscle Wasting

1
Meakins-Christie Laboratories and Translational Research in Respiratory Diseases Program, Research Institute of the McGill University Health Centre; Department of Critical Care, McGill University Health Centre, Montréal, QC H4A 3J1, Canada
2
Division of Experimental Medicine, McGill University, Montréal, QC H4A 3J1, Canada
3
Département des sciences de l’activité physique, Faculté des Sciences, UQAM, Montréal, QC H2X 1Y4, Canada
4
Groupe de recherche en Activité Physique Adaptée, Montréal, QC H2X 1Y4, Canada
5
Département des sciences biologiques, Faculté des Sciences, UQAM, Montréal, QC H2X 1Y4, Canada
6
Centre de Recherche de l’Institut Universitaire de Gériatrie de Montréal, Montréal, QC H3W 1W5, Canada
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work as senior authors.
Cells 2020, 9(6), 1454; https://doi.org/10.3390/cells9061454
Received: 30 April 2020 / Revised: 3 June 2020 / Accepted: 8 June 2020 / Published: 11 June 2020
Sepsis elicits skeletal muscle weakness and fiber atrophy. The accumulation of injured mitochondria and depressed mitochondrial functions are considered as important triggers of sepsis-induced muscle atrophy. It is unclear whether mitochondrial dysfunctions in septic muscles are due to the inadequate activation of quality control processes. We hypothesized that overexpressing Parkin, a protein responsible for the recycling of dysfunctional mitochondria by the autophagy pathway (mitophagy), would confer protection against sepsis-induced muscle atrophy by improving mitochondrial quality and content. Parkin was overexpressed for four weeks in the limb muscles of four-week old mice using intramuscular injections of adeno-associated viruses (AAVs). The cecal ligation and perforation (CLP) procedure was used to induce sepsis. Sham operated animals were used as controls. All animals were studied for 48 h post CLP. Sepsis resulted in major body weight loss and myofiber atrophy. Parkin overexpression prevented myofiber atrophy in CLP mice. Quantitative two-dimensional transmission electron microscopy revealed that sepsis is associated with the accumulation of enlarged and complex mitochondria, an effect which was attenuated by Parkin overexpression. Parkin overexpression also prevented a sepsis-induced decrease in the content of mitochondrial subunits of NADH dehydrogenase and cytochrome C oxidase. We conclude that Parkin overexpression prevents sepsis-induced skeletal muscle atrophy, likely by improving mitochondrial quality and contents. View Full-Text
Keywords: muscle atrophy; septicemia; mitochondria; mitochondrial fusion; mitochondrial fission muscle atrophy; septicemia; mitochondria; mitochondrial fusion; mitochondrial fission
Show Figures

Figure 1

MDPI and ACS Style

Leduc-Gaudet, J.-P.; Mayaki, D.; Reynaud, O.; Broering, F.E.; Chaffer, T.J.; Hussain, S.N.A.; Gouspillou, G. Parkin Overexpression Attenuates Sepsis-Induced Muscle Wasting. Cells 2020, 9, 1454.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop