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TISSUE-SPECIFIC STEM CELLS

Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Promotes Migration of Human Bone Marrow Multipotent Stromal Cells

^aDepartment of Morphology and Embryology, University of Ferrara, Ferrara, Italy;
^bInterdepartmental Center of Regenerative Medicine, University of Udine, Udine, Italy;
^cDepartment of Histology, Embryology and Applied Biology, University of Bologna, Bologna, Italy

Key Words. Tumor necrosis factor-related apoptosis-inducing ligand • Tumor necrosis factor-related apoptosis-inducing ligand receptors • Multipotent precursor • Mesenchymal stem cells • Migration

Correspondence: Correspondence: Giorgio Zauli, M.D., Ph.D., Department of Morphology and Embryology, Human Anatomy Section, University of Ferrara, Via Fossato di Mortara 66, 44100 Ferrara, Italy. Telephone: 39-0532-455579; Fax: 39-0532-207351; e-mail: giorgio.zauli{at}unife.it

Received on May 26, 2008; accepted for publication on August 16, 2008.

First published online in STEM CELLS EXPRESS  September 4, 2008.

Adult multipotent stromal cells (MSCs), also known as mesenchymal stem cells, represent an important source of cells for the repair of a number of damaged tissues. Both bone marrow (BM)-derived and amniotic MSCs expressed detectable surface levels of two (tumor necrosis factor-related apoptosis-inducing ligand receptor 2 [TRAIL-R2] and TRAIL-R4) of four transmembrane TRAIL receptors. Although the best-characterized activity of TRAIL-R2 is the transduction of apoptotic signals, neither recombinant TRAIL (rTRAIL) nor infection with an adenovirus-expressing TRAIL induced cytotoxic effects on MSCs. Moreover, whereas rTRAIL did not affect proliferation or differentiation of MSCs along the osteogenic and adipogenic lineages, it significantly promoted the migration of human MSCs in range of concentrations comparable to that of soluble TRAIL in human plasma (100 pg/ml). Since rTRAIL induced the rapid phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in MSC cultures and pretreatment with pharmacological inhibitors of the ERK1/2 pathway efficiently counteracted the rTRAIL-induced human MSC migration, these data indicate that ERK1/2 is involved in mediating the ability of rTRAIL to stimulate MSC migration. Taking into consideration that the soluble factors able to induce MSC migration have not been extensively characterized, our current data indicate that the TRAIL/TRAIL-R system might play an important role in the biology of MSCs.

Disclosure of potential conflicts of interest is found at the end of this article.