Fibroblasts from long-lived species of mammals and birds show delayed, but prolonged, phosphorylation of ERK

Authors

  • Najoua Elbourkadi,

    1. Department of Pathology and Geriatrics Center, University of Michigan, Ann Arbor, MI, USA
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  • Steven N. Austad,

    1. Barshop Center, University of Texas Health Science Center, San Antonio, TX, USA
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  • Richard A. Miller

    Corresponding author
    1. Department of Pathology and Geriatrics Center, University of Michigan, Ann Arbor, MI, USA
    • Correspondence

      Richard A. Miller, Department of Pathology and Geriatrics Center, University of Michigan, BSRB 3001, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA. Tel.: +734 936 2122; fax: +734 647 9749; e-mail: millerr@umich.edu

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Summary

Fibroblasts from long-lived mutant mice show diminished phosphorylation of the stress-activated protein kinases ERK1/2 after exposure to peroxide, cadmium, or paraquat. We have now evaluated the kinetics of ERK phosphorylation in fibroblasts from long-lived and short-lived species of mammals and birds in response to stress by cadmium or hydrogen peroxide. Fibroblasts from the shorter-lived species of rodents and birds showed rapid induction of ERK phosphorylation, with a decline to basal level within 60 min. In contrast, cells from longer-lived species showed slower and more prolonged activation of ERK phosphorylation. These results suggest that fibroblasts from long-lived species may be less susceptible to the early phases of damage from cadmium or peroxide and suggest that altered kinetics of ERK activity may contribute to their stress resistance properties.

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