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Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment
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Mitochondrial peptides modulate mitochondrial function during cellular senescence.

Su-Jeong Kim1, Hemal H Mehta1, Junxiang Wan1

  • 1Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089, USA.

Aging
|June 11, 2018
PubMed
Summary
This summary is machine-generated.

Mitochondria-derived peptides (MDPs) like humanin and MOTS-c are elevated in senescent cells, influencing mitochondrial function and senescence-associated secretory phenotypes (SASPs). Targeting these peptides may reduce harmful senescence effects.

Keywords:
SASP (senescence-associated secretory phenotype)mitochondriamitochondrial energeticsmitochondrial-derived peptidesmtDNA methylationsenescence

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Area of Science:

  • Cellular Biology
  • Aging Research
  • Mitochondrial Physiology

Background:

  • Cellular senescence, a state of irreversible growth arrest, contributes to age-related diseases.
  • Senescent cells remain metabolically active, producing senescence-associated secretory phenotypes (SASPs).
  • The role of mitochondria and their encoded peptides (MDPs) in senescence is not fully understood.

Purpose of the Study:

  • To investigate mitochondrial physiology and MDPs in senescent human fibroblasts.
  • To explore the impact of specific MDPs (humanin, MOTS-c) on senescent cells.
  • To assess the potential of targeting mitochondrial metabolism to modulate SASP production.

Main Methods:

  • Primary human fibroblasts were induced into senescence via replicative exhaustion, doxorubicin, or hydrogen peroxide.
  • Mitochondrial number, respiration, DNA methylation, and levels of humanin, MOTS-c, SHLP2, and SHLP6 were analyzed.
  • Effects of humanin and MOTS-c administration on senescent cells were evaluated, including JAK pathway involvement.

Main Results:

  • Senescent cells exhibited increased mitochondrial numbers and respiration.
  • Levels of humanin and MOTS-c were elevated in senescent cells.
  • Humanin and MOTS-c partially restored mitochondrial respiration and modulated SASP components, involving the JAK pathway.

Conclusions:

  • Mitochondria-derived peptides humanin and MOTS-c play a role in the bioenergetics of senescent cells.
  • These MDPs influence the production of senescence-associated secretory phenotypes (SASPs).
  • Targeting mitochondrial metabolism and MDPs presents a strategy to mitigate the detrimental effects of cellular senescence.