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Am J Physiol Cell Physiol 289: C521-C530, 2005. First published April 27, 2005; doi:10.1152/ajpcell.00429.2004
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VASCULAR BIOLOGY

Hypoxia alters biophysical properties of endothelial cells via p38 MAPK- and Rho kinase-dependent pathways

Steven S. An,1 Corin M. Pennella,2 Achuta Gonnabathula,2 Jianxin Chen,1 Ning Wang,1 Matthias Gaestel,3 Paul M. Hassoun,4 Jeffrey J. Fredberg,1 and Usamah S. Kayyali2

1Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston; 2Pulmonary and Critical Care Division, Department of Medicine/Tupper Research Institute, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts; 3Institute of Biochemistry, Medical School Hannover, Hannover, Germany; and 4Division of Pulmonary and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland

Submitted 30 August 2004 ; accepted in final form 21 April 2005

Hypoxia alters the barrier function of the endothelial cells that line the pulmonary vasculature, but underlying biophysical mechanisms remain unclear. Using rat pulmonary microvascular endothelial cells (RPMEC) in culture, we report herein changes in biophysical properties, both in space and in time, that occur in response to hypoxia. We address also the molecular basis of these changes. At the level of the single cell, we measured cell stiffness, the distribution of traction forces exerted by the cell on its substrate, and spontaneous nanoscale motions of microbeads tightly bound to the cytoskeleton (CSK). Hypoxia increased cell stiffness and traction forces by a mechanism that was dependent on the activation of Rho kinase. These changes were followed by p38-mediated decreases in spontaneous bead motions, indicating stabilization of local cellular-extracellular matrix (ECM) tethering interactions. Cells overexpressing phospho-mimicking small heat shock protein (HSP27-PM), a downstream effector of p38, exhibited decreases in spontaneous bead motions that correlated with increases in actin polymerization in these cells. Together, these findings suggest that hypoxia differentially regulates endothelial cell contraction and cellular-ECM adhesion.

endothelial barrier; cytoskeleton; actin dynamics; stiffness; tensile stress


Address for reprint requests and other correspondence: U. S. Kayyali, Pulmonary & Critical Care Division, Tufts-New England Medical Center, 750 Washington St. #257, Boston, MA 02111 (e-mail: ukayyali{at}tufts-nemc.org)




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