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Am J Physiol Heart Circ Physiol 284: H2227-H2234, 2003. First published February 6, 2003; doi:10.1152/ajpheart.00920.2002
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Vol. 284, Issue 6, H2227-H2234, June 2003

Integrin shedding as a mechanism of cellular adaptation during cardiac growth

Edie C. Goldsmith1, Wayne Carver1, Alex McFadden1, Jack G. Goldsmith2, Robert L. Price1, Mark Sussman3, Beverly H. Lorell4, Garth Cooper5, and Thomas K. Borg1

1 Department of Developmental Biology and Anatomy, University of South Carolina School of Medicine, Columbia 29208; 2 Department of Chemistry, University of South Carolina, Aiken, South Carolina 29801; 3 Division of Molecular Cardiovascular Biology, The Children's Hospital and Research Foundation, Cincinnati, Ohio 45229-3039; 4 Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215; and 5 Department of Biological Sciences, University of Auckland, Auckland, New Zealand 1020

Integrin-mediated cell-extracellular matrix (ECM) interactions are essential for multiple cellular processes; however, little is known regarding integrin turnover during these events. Recent studies have demonstrated shedding of cell surface molecules and suggested this as a potential mechanism for integrin turnover. Confocal microscopy of mouse hearts under different physiological conditions demonstrated the presence of beta 1-integrin-immunoreactive material in the interstitium. Culture media from neonatal rat cardiac myocytes and fibroblasts contained a 55-kDa fragment of beta 1-integrin. Attachment to ECM components, response to phorbol 12-myristate 13-acetate stimulation, and matrix metalloproteinase inhibition assays demonstrated that fibroblasts responded differently to the fragment compared with myocytes. The beta 1-integrin fragment stimulated myocyte attachment to collagen and the fragment itself bound a variety of ECM proteins. These studies indicate that as myocytes and fibroblasts change size and shape, cellular contacts with the ECM are altered, resulting in the liberation of a beta 1-integrin fragment from the cell surface. Integrin shedding may represent a novel mechanism of rapidly modifying cell-ECM contacts during various cellular processes.

integrins; hypertrophy; extracellular matrix; metalloproteinases


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