Circulation Research. 2004;94:678-685
Published online before print January 22, 2004, doi: 10.1161/01.RES.0000118601.37875.AC
Published online before print January 22, 2004, doi: 10.1161/01.RES.0000118601.37875.AC
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© 2004 American Heart Association, Inc.
Integrative Physiology |
Marrow-Derived Stromal Cells Express Genes Encoding a Broad Spectrum of Arteriogenic Cytokines and Promote In Vitro and In Vivo Arteriogenesis Through Paracrine Mechanisms
From the Cardiovascular Research Institute, Washington Hospital Center, Washington, DC.
Correspondence to Tim Kinnaird, Cardiovascular Research Institute, Room 4B-1, Washington Hospital Center, 110 Irving St, Washington, DC 20010. E-mail tim.kinnaird{at}medstar.net
We recently demonstrated that marrow stromal cells (MSCs) augment collateral remodeling through release of several cytokines such as VEGF and bFGF rather than via cell incorporation into new or remodeling vessels. The present study was designed to characterize the full spectrum of cytokine genes expressed by MSCs and to further examine the role of paracrine mechanisms that underpin their therapeutic potential. Normal human MSCs were cultured under normoxic or hypoxic conditions for 72 hours. The gene expression profile of the cells was determined using Affymetrix GeneChips representing 12 000 genes. A wide array of arteriogenic cytokine genes were expressed at baseline, and several were induced >1.5-fold by hypoxic stress. The gene array data were confirmed using ELISA assays and immunoblotting of the MSC conditioned media (MSCCM). MSCCM promoted in vitro proliferation and migration of endothelial cells in a dose-dependent manner; anti-VEGF and anti-FGF antibodies only partially attenuated these effects. Similarly, MSCCM promoted smooth muscle cell proliferation and migration in a dose-dependent manner. Using a murine hindlimb ischemia model, murine MSCCM enhanced collateral flow recovery and remodeling, improved limb function, reduced the incidence of autoamputation, and attenuated muscle atrophy compared with control media. These data indicate that paracrine signaling is an important mediator of bone marrow cell therapy in tissue ischemia, and that cell incorporation into vessels is not a prerequisite for their effects.
Key Words: marrow stromal cells • arteriogenesis • bone marrow cells • cytokines
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T. Kinnaird, E. Stabile, M. S. Burnett, and S. E. Epstein Bone Marrow-Derived Cells for Enhancing Collateral Development: Mechanisms, Animal Data, and Initial Clinical Experiences Circ. Res., August 20, 2004; 95(4): 354 - 363. [Abstract] [Full Text] [PDF]
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M. D. Schuster, A. A. Kocher, T. Seki, T. P. Martens, G. Xiang, S. Homma, and S. Itescu Myocardial neovascularization by bone marrow angioblasts results in cardiomyocyte regeneration Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H525 - H532. [Abstract] [Full Text] [PDF]
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M. F. Pittenger and B. J. Martin Mesenchymal Stem Cells and Their Potential as Cardiac Therapeutics Circ. Res., July 9, 2004; 95(1): 9 - 20. [Abstract] [Full Text] [PDF]
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M. Heil, T. Ziegelhoeffer, B. Mees, and W. Schaper A Different Outlook on the Role of Bone Marrow Stem Cells in Vascular Growth: Bone Marrow Delivers Software not Hardware Circ. Res., March 19, 2004; 94(5): 573 - 574. [Full Text] [PDF]
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