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*Department of Experimental Endocrinology,
Department of Biochemistry, and
Department of Pathology, University of Crete, School of Medicine, Heraklion, Greece; and
UMR976 INSERM, Hôpital St Louis, Paris, France
Adipose tissue represents a rich source of multipotent stem cells. Mesenchymal cells, isolated from this source, can differentiate to other cell types in vitro and therefore can be used for a number of regenerative therapies. Our view of adipose tissue has recently changed, establishing adipocytes as new members of the immune system, as they produce a number of proinflammatory cytokines (such as IL-6 and TNF
and chemokines, in addition to adipokines (leptin, adiponectin, resistin) and molecules associated with the innate immune system. In this paper, we report the differential expression of TNF-superfamily members B cell activating factor of the TNF Family (BAFF), a proliferation inducing ligand (APRIL), and TNF-like weak inducer of apoptosis (TWEAK) in immature-appearing and mature adipocytes and in benign and malignant adipose tissue-derived tumors. These ligands act through their cognitive receptors, BAFF receptor, transmembrane activator and calcium signal-modulating cyclophilic ligand (TACI), B cell maturation Ag (BCMA), and fibroblast growth factor-inducible 14 (Fn14), which are also expressed in these cells. We further report the existence of functional BCMA, TACI, and Fn14 receptors and their ligands BAFF, APRIL, and TWEAK on adipose tissue-derived mesenchymal cells, their interaction modifying the rate of adipogenesis. Our data integrate BAFF, APRIL, and TWEAK and their receptors BCMA, TACI, and Fn14 as novel potential mediators of adipogenesis, in addition to their specific role in immunity, and define immature and mature adipocytes as source of immune mediators.
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.
1 This work was supported by grants from INSERM and the University of Crete Research Committee.
2 Current address: Laboratoire J.-C. Heuson de Cancérologie Mammaire, Institut Jules Bordet-Centre des Tumeurs de l’ULB, Brussels, 1000, Belgium.
3 Address correspondence and reprint requests to Dr. Elias Castanas, University of Crete, School of Medicine, Laboratory of Experimental Endocrinology, P.O. Box 2208, Heraklion, 71003, Greece. E-mail address: castanas{at}med.uoc.gr or Dr. Andreas Tsapis, UMR976 INSERM, Hôpital St Louis, 1, Av. Claude Vellefaux, Paris, 75010, France. E-mail address: andreas.tsapis{at}inserm.fr
4 Abbreviations used in this paper: BAFF, B cell activating factor of the TNF family; APRIL, a proliferation inducing ligand; TWEAK, TNF-like weak inducer of apoptosis; TACI, transmembrane activator and calcium signal-modulating cytophilic ligand; BCMA, B cell maturation Ag; BAFF-R, BAFF receptor; Fn14, fibroblast growth factor-inducible 14; LPL, lipoprotein lipase; ADMC, adipose tissue-derived mesenchymal cell; MSC, mesenchymal stem cell; qRT-PCR, quantitative RT-PCR; SF, Superfamily.
5 The online version of this article contains supplemental material.
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