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

Wen Hui Tsai, Shu Lien Lai, I. Ting Li, Hong Yu Chien, Chung Hung Shih, Yu Ru Kou, Hui Chi Hsu

Research output: Contribution to journalArticle

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)551-557
Number of pages7
JournalJournal of Cellular Biochemistry
Volume114
Issue number3
DOIs
Publication statusPublished - Mar 2013

Fingerprint

Annexins
Endothelial cells
Tretinoin
Annexin A1
Cell Communication
Adhesives
Dexamethasone
Endothelial Cells
Adhesion
Cell-Derived Microparticles
Neutralizing Antibodies
Anti-Inflammatory Agents

Keywords

  • ACUTE PROMYELOCYTIC LEUKEMIA
  • ALL-TRANS RETINOIC ACID
  • ANNEXIN A1
  • DEXAMETHASONE
  • DIFFERENTIATION SYNDROME
  • MICROPARTICLES

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

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. / Tsai, Wen Hui; Lai, Shu Lien; Li, I. Ting; Chien, Hong Yu; Shih, Chung Hung; Kou, Yu Ru; Hsu, Hui Chi.

In: Journal of Cellular Biochemistry, Vol. 114, No. 3, 03.2013, p. 551-557.

Research output: Contribution to journalArticle

@article{4d16f6e8e93f4f73b4f4cb641dc7bbd5,
title = "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",
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.",
keywords = "ACUTE PROMYELOCYTIC LEUKEMIA, ALL-TRANS RETINOIC ACID, ANNEXIN A1, DEXAMETHASONE, DIFFERENTIATION SYNDROME, MICROPARTICLES",
author = "Tsai, {Wen Hui} and Lai, {Shu Lien} and Li, {I. Ting} and Chien, {Hong Yu} and Shih, {Chung Hung} and Kou, {Yu Ru} and Hsu, {Hui Chi}",
year = "2013",
month = "3",
doi = "10.1002/jcb.24394",
language = "English",
volume = "114",
pages = "551--557",
journal = "Journal of Cellular Biochemistry",
issn = "0730-2312",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - 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

AU - Tsai, Wen Hui

AU - Lai, Shu Lien

AU - Li, I. Ting

AU - Chien, Hong Yu

AU - Shih, Chung Hung

AU - Kou, Yu Ru

AU - Hsu, Hui Chi

PY - 2013/3

Y1 - 2013/3

N2 - 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.

AB - 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.

KW - ACUTE PROMYELOCYTIC LEUKEMIA

KW - ALL-TRANS RETINOIC ACID

KW - ANNEXIN A1

KW - DEXAMETHASONE

KW - DIFFERENTIATION SYNDROME

KW - MICROPARTICLES

UR - http://www.scopus.com/inward/record.url?scp=84872773100&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84872773100&partnerID=8YFLogxK

U2 - 10.1002/jcb.24394

DO - 10.1002/jcb.24394

M3 - Article

C2 - 22991072

AN - SCOPUS:84872773100

VL - 114

SP - 551

EP - 557

JO - Journal of Cellular Biochemistry

JF - Journal of Cellular Biochemistry

SN - 0730-2312

IS - 3

ER -