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Originally published In Press as doi:10.1074/jbc.M306951200 on August 7, 2003

J. Biol. Chem., Vol. 278, Issue 43, 42307-42312, October 24, 2003
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Bone Marrow Transplantation Reveals the in Vivo Expression of the Mitochondrial Uncoupling Protein 2 in Immune and Nonimmune Cells during Inflammation*

Marie-Clotilde Alves-Guerra{ddagger}, Sophie Rousset{ddagger}, Claire Pecqueur{ddagger}, Ziad Mallat§, Julie Blanc§, Alain Tedgui§, Fredéric Bouillaud{ddagger}, Anne-Marie Cassard-Doulcier{ddagger}, Daniel Ricquier{ddagger}, and Bruno Miroux{ddagger}

From the {ddagger}CNRS UPR 9078, Faculté de Médecine Necker-Enfants Malades, 75730 Paris Cedex 15, France and §INSERM U541, Hôpital Lariboisière, 75475 Paris Cedex 10, France

The mitochondrial uncoupling protein 2 (UCP2) is expressed in spleen, lung, intestine, white adipose tissue, and immune cells. Bone marrow transplantation in mice was used to assess the contribution of immune cells to the expression of UCP2 in basal condition and during inflammation. Immune cells accounted for the total amount of UCP2 expression in the spleen, one-third of its expression in the lung, and did not participate in its expression in the intestine. LPS injection stimulated UCP2 expression in lung, spleen, and intestine in both immune and non-immune cells. Successive injections of LPS and dexamethasone or N-acetyl-cysteine prevented the induction of UCP2 in all three tissues, suggesting that oxygen free radical generation plays a role in UCP2 regulation. Finally, both previous studies and our data show that there is down-regulation of UCP2 in immune cells during their activation in the early stages of the LPS response followed by an up-regulation in UCP2 during the later stages to protect all cells against oxidative stress.


Received for publication, June 30, 2003 , and in revised form, July 25, 2003.

* This work was supported by INSERM, CNRS, Institut de Recherches Servier (to D. R.), Action Concertée Incitative, Ministère de la Recherche, France (to D. R. and A. T.), and GlaxoSmithKline (to M.-C. A.-G.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: CNRS UPR 9078, Faculté de Médecine Necker-Enfants Malades, 156 rue de Vaugirard, 75730 Paris Cedex 15, France. Tel.: 00-331-4061-5671; Fax: 00-331-4061-5673; E-mail: miroux{at}necker.fr.


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