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Increase of oxidatively modified protein is associated with a decrease of proteasome activity and content in aging

I Petropoulos1, M Conconi, X Wang

  • 1Laboratoire de Biologie et Biochimie Cellulaire du Vieillissement, Université Denis Diderot, Paris, France.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|May 20, 2000
PubMed
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Aging epidermal cells show increased damaged proteins and decreased proteasome function. This proteasome downregulation in aged cells and replicative senescence leads to protein accumulation, impacting skin health.

Area of Science:

  • Cellular biology
  • Dermatology
  • Biochemistry

Background:

  • The aging process involves cellular damage and impaired protein homeostasis.
  • The proteasome is crucial for degrading damaged proteins.

Purpose of the Study:

  • To investigate the role of proteasome function in epidermal cell aging.
  • To determine if proteasome activity declines with age and replicative senescence.

Main Methods:

  • Assaying modified protein levels (oxidized, glycated, 4-hydroxy-2-nonenal) in epidermal cells from donors of varying ages.
  • Measuring proteasome activity (chymotrypsin-like, peptidylglutamyl-peptide hydrolase) and content via immunoblotting and ELISA.
  • Assessing proteasome function in cultured keratinocytes during serial passaging.
  • Correlating proteasome content with the aging marker senescence-associated β-galactosidase.

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Main Results:

  • Epidermal cells from older donors exhibited higher levels of oxidized, glycated, and 4-hydroxy-2-nonenal-modified proteins.
  • Proteasome activity, specifically chymotrypsin-like and peptidylglutamyl-peptide hydrolase, decreased in aging keratinocytes.
  • A reduction in proteasome content was observed in aging cells, correlating with decreased activity.
  • Serial passaging of keratinocytes led to decreased proteasome activity and content.
  • An inverse relationship was found between senescence-associated β-galactosidase and proteasome content in both cell cultures and skin.

Conclusions:

  • Proteasome function is downregulated in aging epidermal cells both in vivo and in vitro.
  • This age-related decline in proteasome activity contributes to the accumulation of modified proteins.
  • Proteasome downregulation is associated with replicative senescence and cellular aging in keratinocytes.