The peptide methionine sulfoxide reductases, MsrA and MsrB (hCBS‐1), are downregulated during replicative senescence of human WI‐38 fibroblasts

FEBS Letters

Cintrat, Jean-Christophe¹  Friguet, Bertrand²  Picot, Cédric R²  Petropoulos, Isabelle²  Perichon, Martine² 

[1] Service des Molécules Marquées, Département de Biologie Cellulaire et Moléculaire, CEA/Saclay, 91191 Gif-sur-Yvette Cedex, France;Laboratoire de Biologie et Biochimie Cellulaire du Vieillissement, Université Paris 7-Denis Diderot, 2 place Jussieu, Tour 33-23, 1 étage, CC 7128, 75251 Paris Cedex 05, France

关键词: Senescence;    Protein oxidation;    Methionine sulfoxide;    Protein repair;    Oxidative stress;    ROS;    reactive oxygen species;    PMSR;    peptide methionine sulfoxide reductase;    MsrA;    peptide methionine sulfoxide reductase A;    MsrB;    peptide methionine sulfoxide reductase B;    SA;    senescence-associated;    CPD;    cumulative population doubling;    Met(O);    methionine sulfoxide;   

DOI  :  10.1016/S0014-5793(03)01530-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In contrast to other oxidative modifications of amino acids, methionine sulfoxide can be enzymatically reduced back to methionine in proteins by the peptide methionine sulfoxide reductase system, composed of MsrA and MsrB. The expression of MsrA and one member of the MsrB family, hCBS-1, was analyzed during replicative senescence of WI-38 human fibroblasts. Gene expression decreased for both enzymes in senescent cells compared to young cells, and this decline was associated with an alteration in catalytic activity and the accumulation of oxidized proteins during senescence. These results suggest that downregulation of MsrA and hCBS-1 can alter the ability of senescent cells to cope with oxidative stress, hence contributing to the age-related accumulation of oxidative damage.

【 授权许可】

Unknown