Identification of CXCR4 as a New Nitric Oxide-Regulated Gene in Human CD34+ Cells (original) (raw)

Journal Article

,

INSERM U790, Institut Gustave Roussy, PR1

, Villejuif,

France

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,

INSERM U790, Institut Gustave Roussy, PR1

, Villejuif,

France

Search for other works by this author on:

,

INSERM U790, Institut Gustave Roussy, PR1

, Villejuif,

France

Search for other works by this author on:

,

INSERM U790, Institut Gustave Roussy, PR1

, Villejuif,

France

Search for other works by this author on:

,

INSERM U790, Institut Gustave Roussy, PR1

, Villejuif,

France

Search for other works by this author on:

INSERM U790, Institut Gustave Roussy, PR1

, Villejuif,

France

Correspondence: Fawzia Louache, Ph.D., INSERM U790, Institut Gustave Roussy, PR1, 39 Rue Camille Desmoulins, 94805 Villejuif, France. Telephone: 33 1 42 11 42 33; Fax: 33 1 42 11 52 40; e-mail: fawl@igr.fr

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Accepted:

22 September 2006

Published:

05 October 2006

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Yanyan Zhang, Monika Wittner, Hakim Bouamar, Peggy Jarrier, William Vainchenker, Fawzia Louache, Identification of CXCR4 as a New Nitric Oxide-Regulated Gene in Human CD34+ Cells, Stem Cells, Volume 25, Issue 1, January 2007, Pages 211–219, https://doi.org/10.1634/stemcells.2006-0468
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Abstract

As an intracellular second messenger, nitric oxide (NO) is increasingly implicated in the control of transcriptional machinery and gene expression. Here, we show that cell surface expression of CXCR4 on CD34+ cells was increased in a dose- and time-dependent manner in response to NO donors. Augmented surface expression was correlated with an increase in CXCR4 mRNA level. A specific NO scavenger prevented the elevation in CXCR4 mRNA caused by NO donors, suggesting a direct signaling action mediated by NO on CXCR4 transcription. NO treatment had no significant effect on CXCR4 mRNA stability. However, induction of CXCR4 mRNA by NO was still observed in conditions in which initiation of translation was inhibited, suggesting that the NO effect must be mediated by a pre-existing protein. CXCR4 mRNA induction did not involve cGMP (guanosine 3′, 5′-cyclic monophosphate) generation but was most likely mediated via oxidation of intracellular protein thiols. Finally, CD34+ cells pretreated with NO donors exhibited an increased chemotactic response. This study demonstrates that the NO pathway can modulate CXCR4 expression in human CD34+ cells and suggests that NO may play a critical role in the trafficking of hematopoietic progenitors.

Copyright © 2007 AlphaMed Press

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open\_access/funder\_policies/chorus/standard\_publication\_model)

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