Endothelial f-actin depolymerization enables leukocyte transmigration |
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Authors: | Laura Isac Gerold Thoelking Albrecht Schwab Hans Oberleithner Christoph Riethmuller |
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Institution: | 1.Institute of Physiology II,University of Münster,Münster,Germany;2.Rheumatology Unit,University Clinic of Bucharest,Bucharest,Romania;3.Medical Clinic D,University Clinic of Münster,Münster,Germany;4.Serend-ip GmbH,Technology Center,Münster,Germany |
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Abstract: | A demanding task of medicine is to understand and control the immune system. Central players in the cellular immune response
are the leukocytes that leave the blood stream for host defense. Endothelial cells limit the emigration rate of leukocytes.
Being located between blood and tissues, they permit or deny the passage. The exact mechanism of this process called diapedesis
is not solved yet. Leukocytes can principally traverse either between cells (paracellularly) or directly through an individual
endothelial cell (transcellularly). The transcellular way has recently gained experimental support, but it is not clear how
the endothelial cytoskeleton manages to open and close a transmigratory channel. Atomic force microscopy was used to investigate
the endothelial cytoskeleton. In order to directly access the leukocyte–endothelial interaction site, we applied a special
protocol (“nanosurgery”). As a result, the endothelial cell turned out to become softer in a confined region strictly underneath
the leukocyte. Fluorescence microscopy confirmed a depolymerization of the f-actin strands at the invasion site. Leukocytes
dramatically rearrange the endothelial cytoskeleton to form transmigratory channels. |
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