Get access

Oxidative preconditioning promotes bone marrow mesenchymal stem cells migration and prevents apoptosis

Authors

  • ShiYong Li,

    1. Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Zhongshan ErLu 74, Guangzhou 510080, China
    Search for more papers by this author
  • YuBin Deng,

    Corresponding author
    1. Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Zhongshan ErLu 74, Guangzhou 510080, China
      Tel.: +86 20 88385762. E-mail addresses: dengyub@mail.sysu.edu.cn
    Search for more papers by this author
  • JianQiang Feng,

    1. Department of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China
    Search for more papers by this author
  • WeiBiao Ye

    1. Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Zhongshan ErLu 74, Guangzhou 510080, China
    Search for more papers by this author

Tel.: +86 20 88385762. E-mail addresses: dengyub@mail.sysu.edu.cn

Abstract

Reactive oxygen species (ROS) play essential roles in apoptosis and in the regulation of several transcription factors under both physiological and pathological conditions. However, the effects of ROS on MSCs are not well known, and therefore we have investigated the effects of preconditioning with hydrogen peroxide (H2O2) on the level of expression of the chemokine receptor, CXCR4, stromal cell-derived factor-1α (SDF-1α)-dependent migration and apoptosis in MSCs. Preconditioning with 20 μM H2O2 significantly increased the level of expression of CXCR4 mRNA and protein, and MSCs migration toward SDF-1α; increased expression of CXCR4 and SDF-1α-induced MSCs migration was attenuated by extracellular signal-regulated kinase (ERK) inhibitor PD98059. Preconditioning with 20 μM H2O2 significantly protected MSCs against apoptosis induced by 500 μM H2O2. These results suggest that preconditioning with H2O2 can increase MSCs migration toward SDF-1α and protect MSCs against apoptosis.

Get access to the full text of this article

Ancillary