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Journal of Cellular Biochemistry

Annexin A1 mediates the anti-adhesive effects of dexamethasone during the cell–cell interaction between the all-trans retinoic acid-treated acute promyelocytic leukemic cells and endothelial cells

Authors

  • Wen-Hui Tsai,

    1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
    2. Department of Respiratory Therapy, Taipei Medical University, Taipei, Taiwan, Republic of China
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  • Shu-Lien Lai,

    1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
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  • I-Ting Li,

    1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
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  • Hong-Yu Chien,

    1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
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  • Chung-Hung Shih,

    1. Department of Respiratory Therapy, Taipei Medical University, Taipei, Taiwan, Republic of China
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  • Yu Ru Kou,

    1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
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  • Hui-Chi Hsu MD

    Corresponding author
    1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
    2. Division of General Medicine and Division of Hematology and Oncology, Department of Medicine, Taipei-Veterans General Hospital, Taipei, Taiwan, Republic of China
    3. Department of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
    • Division of General Medicine, Department of Medicine, Taipei Veterans General Hospital, 201, Sec. 2, Shih-Pai Road, Taipei, Taiwan 11217, Republic of China.
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  • All authors declare that there is no conflict of interest.

Abstract

Annexin A1 (AnxA1) is an important anti-inflammatory mediator during granulocytic differentiation in all trans-retinoic acid (ATRA) treated acute promyelocytic leukemic (APL) cells. Dexamethasone has been used successfully to prevent complications in ATRA-treated APL patients, although its mechanism of action is still not clear. In the present study, we have examined the effect of dexamethasone on the modulation of AnxA1 in ATRA-APL NB4 (ATRA-NB4) cells, ATRA-NB4 cells-derived microparticles (MPs) and its role during cell–cell interaction between ATRA-NB4 cells and endothelial cells. Our results have shown that dexamethasone can inhibit the percentage of ATRA-NB4 cells expressing surface AnxA1 and its receptor FPR2/ALX in a time-dependent manner based on flow cytometric analysis. However, dexamethasone treatment of ATRA-NB4 cells has no significant effect on the level of AnxA1 mRNA, the total cellular level of AnxA1 protein or the release of AnxA1 from these cells, as determined by RT-PCR, Western blotting, and ELISA, respectively. Further studies demonstrate that dexamethasone is able to significantly inhibit the adhesion of ATRA-NB4 cells to endothelial cells, and this anti-adhesive effect can be inhibited if the cells were pre-treated with a neutralizing antibody specific for AnxA1. Finally, dexamethasone also enhances the release of AnxA1-containing MPs from ATRA-NB4 cells which can in turn prevent the adhesion of the ATRA-NB4 cells to endothelial cells. We conclude that biologically active AnxA1 originating from dexamethasone-treated ATRA-APL cells and their MPs plays an anti-adhesive effect and this contributes to inhibit the adhesion of ATRA-APL cell to endothelial cells. J. Cell. Biochem. 114: 551–557, 2013. © 2012 Wiley Periodicals, Inc.

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