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TISSUE-SPECIFIC STEM CELLS

Adhesive Interactions Between Human Neural Stem Cells and Inflamed Human Vascular Endothelium Are Mediated by Integrins

^aBurnham Institute for Medical Research, La Jolla, California, USA;
^bLa Jolla Institute for Molecular Medicine, San Diego, California, USA

Key Words. Adhesion molecules • Rolling • Neural stem cell • Integrins • Homing • Endothelial cell • Cell trafficking

Correspondence: Evan Y. Snyder, M.D., Ph.D., Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, California 92037, USA. Telephone: 58-646-3158; Fax: 858-713-6273; e-mail: esnyder{at}burnham.org or Sophia K. Khaldoyanidi, M.D., Ph.D. La Jolla Institute for Molecular Medicine, 4570 Executive Drive, San Diego, California 92121, USA. Telephone: 858-587-8788; Fax: 858-587-6742; e-mail: sophia{at}ljimm.org

Received November 16, 2005; accepted for publication May 30, 2006.


Understanding the mechanisms by which stem cells home precisely to regions of injury or degeneration is of importance to both basic and applied regenerative medicine. Optimizing regenerative processes may depend on identifying the range of molecules that subserve stem cell trafficking. The "rolling" of extravasating cells on endothelium under conditions of physiological flow is the first essential step in the homing cascade and determines cell adhesion and transmigration. Using a laminar flow chamber to simulate physiological shear stress, we explored an aspect of this process by using human neural stem cells (hNSCs). We observed that the interactions between hNSCs and tumor necrosis factor- (TNF-)-stimulated human endothelium (simulating an inflamed milieu) are mediated by a subclass of integrins—2, 6, and ß1, but not 4, v, or the chemokine-mediated pathway CXCR4-stromal cell-derived factor-1—suggesting not only that the mechanisms mediating hNSC homing via the vasculature differ from the mechanisms mediating homing through parenchyma, but also that each step invokes a distinct pathway mediating a specialized function in the hNSC homing cascade. (TNF- stimulation also upregulates vascular cell adhesion molecule-1 expression on the hNSCs themselves and increases NSC-endothelial interactions.) The selective use of integrin subgroups to mediate homing of cells of neuroectodermal origin may also be used to ensure that cells within the systemic circulation are delivered to the pathological region of a given organ to the exclusion of other, perhaps undesired, organs.

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