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Article type: Research Article
Authors: Elson, E.L.a | Pasternak, C.a; * | Liu, Z.-Y.a; ** | Young, J.-I.a | Schwab III, B.a | Worthen, G.S.b | Downey, G.b; *** | Michaels, R.a | McConnaughey, W.B.a | McDaniel, M.c | Wolf, B.c | Zahalak, G.I.d
Affiliations: [a] Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA | [b] Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, and University of Colorado School of Medicine, Denver, CO 80206, USA | [c] Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA | [d] Department of Mechanical Engineering, Washington University, St. Louis, MO 63130, USA
Note: [*] Current address: Department of Cell Biology, Stanford University, Stanford, CA 94305, USA.
Note: [**] Current address: Department of Biochemistry, USUHS, School of Medicine, Bethesda MD 20814 USA.
Note: [***] Current address: Department of Medicine, Respiratory Division, University of Toronto, Ontario, Canada M5S 1A8.
Note: [] Accepted by: Editor H.J. Meiselman
Abstract: Different kinds of leukocytes undergo cytoskeleton-dependent mechanical responses associated wit their specific physiological functions. We have investigated cellular stiffening of several types of leukocytes using a method which measures the force resisting cellular indentation. We have found that lymphocytes stiffen in response to crosslinking cell surface antigens in a process associated with the much studied capping and patching processes. Further studies of myosin-deficient mutants of the ameba Dictyostelium discoideum suggest that this stiffening process results from a myosin dependent contractile process. Rat basophilic leukemia cells and pancreatic islet cells stiffen when triggered to secrete. The function of these cytoskeleton dependent processes is now unknown, but, at least in the islet cells, may be related to a regulation of the rate of secretion. Primary neutrophils stiffen in response to the chemotactic agent, fMet-Leu-Phe. This stiffening may be responsible for retention of these cells in the pulmonary microcirculation during response to inflammation. These observations pose the challenge of determining the structural basis, mechanism, and physiological function of each of these cellular responses.
Keywords: Cell Stiffening, Patching, Capping, Secretion, Cytoskeleton, Viscoelasticity
DOI: 10.3233/BIR-1990-27605
Journal: Biorheology, vol. 27, no. 6, pp. 849-858, 1990
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