Methionine restriction slows down senescence in human diploid fibroblasts

Summary Methionine restriction (MetR) extends lifespan in animal models including rodents. Using human diploid fibroblasts (HDF), we report here that MetR significantly extends their replicative lifespan, thereby postponing cellular senescence. MetR significantly decreased activity of mitochondrial...

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Bibliographic Details
Published in:Aging cell 2014-12, Vol.13 (6), p.1038-1048
Main Authors: Kozieł, Rafał, Ruckenstuhl, Christoph, Albertini, Eva, Neuhaus, Michael, Netzberger, Christine, Bust, Maria, Madeo, Frank, Wiesner, Rudolf J., Jansen‐Dürr, Pidder
Format: Article
Language:English
Subjects:
Age Factors
Amino acids
Animals
B cells
cellular senescence
Diploidy
Disease Models, Animal
fibroblast
Fibroblasts - cytology
Fibroblasts - drug effects
Fibroblasts - metabolism
Humans
Medical research
methionine
Methionine - administration & dosage
Methionine - deficiency
Methionine - metabolism
mitochondria
Mitochondria - metabolism
Original
oxidative stress
Oxidative Stress - physiology
Protein biosynthesis
Rodents
Senescence
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Summary:Summary Methionine restriction (MetR) extends lifespan in animal models including rodents. Using human diploid fibroblasts (HDF), we report here that MetR significantly extends their replicative lifespan, thereby postponing cellular senescence. MetR significantly decreased activity of mitochondrial complex IV and diminished the accumulation of reactive oxygen species. Lifespan extension was accompanied by a significant decrease in the levels of subunits of mitochondrial complex IV, but also complex I, which was due to a decreased translation rate of several mtDNA‐encoded subunits. Together, these findings indicate that MetR slows down aging in human cells by modulating mitochondrial protein synthesis and respiratory chain assembly.
ISSN:1474-9718
1474-9726
DOI:10.1111/acel.12266