CCHFV GP38 triggers endothelial hyperpermeability and endothelial glycocalyx layer (EGL) component disruption (IMAGE)

US Army Medical Research Institute of Infectious Diseases

CCHFV GP38 triggers endothelial hyperpermeability and endothelial glycocalyx layer (EGL) component disruption

Caption

Human pulmonary microvascular endothelial cells (HPMECs) were treated with GP38 and were stained for endothelial glycocalyx layer component sialic acid by immunofluorescence. Measurement of the integrity of EGL component sialic acid revealed significant reductions in the amounts on the surface of HPMEC after GP38 treatment, supporting the hypothesis that GP38 triggers endothelial hyperpermeability and the disruption of EGL components.

Credit

Felix Pahmeier, University of California, Berkeley

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