rickettsiae induce microvascular hyperpermeability via phosphorylation of ve-cadherins evidence from atomic force microscopy and biochemical studiesrickettsiae诱导的研究通过磷酸化ve-cadherins证据从原子力显微镜和生化研究.pdfVIP

Rickettsiae Induce Microvascular Hyperpermeability via Phosphorylation of VE-Cadherins: Evidence from Atomic Force Microscopy and Biochemical Studies 1,2 3 1 1 1 1,2 1 Bin Gong *, Liang Ma , Yan Liu , Qinyu Gong , Thomas Shelite , Donald Bouyer , Paul J. Boor , Yong Sun Lee4, Andres Oberhauser3,4,5 1 Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America, 2 Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America, 3 Department of Neurosciences and Cell Biology, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America, 4 Department of Biochemistry and Molecular Biology, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America, 5 Sealy Center for Structural Biology and Molecular Biophysics, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America Abstract The most prominent pathophysiological effect of spotted fever group (SFG) rickettsial infection of microvascular endothelial cells (ECs) is an enhanced vascular permeability, promoting vasogenic cerebral edema and non-cardiogenic pulmonary edema, which are responsible for most of the morbidity and mortality in severe cases. To date, the cellular and molecular mechanisms by which SFG Rickettsia increase EC permeability are largely unknown. In the present study we used atomic force microscopy (AFM) to study the interactive forces between vascular endothelial (VE)-cadherin and human cerebral microvascular EC infected with R. montanensis, which is genetically similar to R. rickettsii a