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Tocopherol-mediated modulation of age-related changes in microglial cells: Turnover of extracellular oxidized protein material

journal contribution
posted on 2015-03-04, 12:10 authored by Alexandra StolzingAlexandra Stolzing, Rebecca Widmer, Tobias Jung, Peter Voss, Tilman Grune
Proteins accumulate during aging and form insoluble protein aggregates. Microglia are responsible for their removal from the brain. During aging, changes within the microglia might play a crucial role in the malfunctioning of these cells. Therefore, we isolated primary microglial cells from adult rats and compared their activation status and their ability to degrade proteins to that of microglial cells isolated from newborn animals. The ability of adult microglial cells to degrade proteins is substantially decreased. However, the preincubation of microglial cells with vitamin E improves significantly the degradation of such modified proteins. The degradation of proteins from apoptotic vesicles is decreased in microglia isolated from adult rats. This might be the result of a suppression of the CD36 receptor due to vitamin E treatment. We concluded that microglial cells isolated from adult organisms have different metabolic properties and seem to be a more valuable model to study age-related diseases.

Funding

GK1033 and SFB575

History

School

  • Mechanical, Electrical and Manufacturing Engineering

Published in

Free Radical Biology and Medicine

Volume

40

Issue

12

Pages

2126 - 2135

Citation

STOLZING, A. ... et al., 2006. Tocopherol-mediated modulation of age-related changes in microglial cells: Turnover of extracellular oxidized protein material. Free Radical Biology and Medicine, 40 (12), pp. 2126 - 2135.

Publisher

© Elsevier Inc.

Version

  • VoR (Version of Record)

Publisher statement

This work is made available according to the conditions of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. Full details of this licence are available at: https://creativecommons.org/licenses/by-nc-nd/4.0/

Publication date

2006

Notes

Closed access

ISSN

0891-5849

Other identifier

S0891584906001183

Language

  • en

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