2012
DOI: 10.1007/s00705-012-1245-7
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Dysregulation of the β3 integrin-VEGFR2 complex in Hantaan virus–directed hyperpermeability upon treatment with VEGF

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Cited by 18 publications
(14 citation statements)
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“…Another study found that VEGF binding to VEGF receptor 2 (VEGFR2) may result in dissociation of VEGF-R2 from VE-cadherin, VE-cadherin activation, internalization, and degradation, that VEGF addition to ANDV- and HTNV-infected endothelial cells may induce the hyperphosphorylation of VEGFR2, and that concomitant with the VEGFR2 hyperphosphorylation, VE-cadherin may be internalized to intracellular vesicles within ANDV- or HTNV- infected endothelial cells (Gorbunova et al, 2010 ). Wang et al ( 2012b ) found the interaction between β3 integrin and VEGFR2 and the formation of a functional complex and that the signaling through this complex caused cytoskeletal reorganization, which was an important mechanisms underlying hyperpermeability. They also found that VEGF remarkably enhanced HTNV-directed permeability and the disruption of junctional organizations in an endothelial cell (EC) monolayer at 3 days postinfection.…”
Section: Pathogenesis Of Hfrsmentioning
confidence: 99%
“…Another study found that VEGF binding to VEGF receptor 2 (VEGFR2) may result in dissociation of VEGF-R2 from VE-cadherin, VE-cadherin activation, internalization, and degradation, that VEGF addition to ANDV- and HTNV-infected endothelial cells may induce the hyperphosphorylation of VEGFR2, and that concomitant with the VEGFR2 hyperphosphorylation, VE-cadherin may be internalized to intracellular vesicles within ANDV- or HTNV- infected endothelial cells (Gorbunova et al, 2010 ). Wang et al ( 2012b ) found the interaction between β3 integrin and VEGFR2 and the formation of a functional complex and that the signaling through this complex caused cytoskeletal reorganization, which was an important mechanisms underlying hyperpermeability. They also found that VEGF remarkably enhanced HTNV-directed permeability and the disruption of junctional organizations in an endothelial cell (EC) monolayer at 3 days postinfection.…”
Section: Pathogenesis Of Hfrsmentioning
confidence: 99%
“…In fact, VEGF binding to VEGFR2 on endothelial cells could result in phosphorylation of the receptors to transduce the major signals for angiogenesis [35, 36]. However, the Hantaviruses infection could block the function of the complex of VEGFR2 and β 3 integrin, which may contribute to cytoskeletal reorganization in an HTNV-induced hyperpermeability response to VEGF [37, 38]. Endothelial cell monolayers are not permeabilized by Hantavirus infection alone, and pathogenic Hantaviruses direct endothelium hyperpermeability by sensitizing endothelial cells hyperresponsive to VEGF, or indirectly through the induction of nitric oxide and prostacyclin, and this alters the fluid barrier function of endothelial cell adherence junctions, resulting in enhanced paracellular permeability [3943].…”
Section: Discussionmentioning
confidence: 99%
“…Integrin ανβ3, experimentally proven to be the receptor for hantavirus infection, is abundantly present on the surface of endothelial cells ( Gavrilovskaya et al, 1999 ; Song et al, 2005 ). Infection with pathogenic hantaviruses is suggested to result in the loss of function of the ανβ3 integrin ( Wang et al, 2012 ), but also an increased ανβ3 expression on cultured endothelial cells and platelets has been observed ( Liu et al, 2008 ). Furthermore Gavrilovskaya et al (2010) studied the adherence of quiescent platelets to Sin Nombre and Hantaan virus infected endothelial cells seems to be the result of virus binding to the ανβ3 integrin present on platelets ( Gavrilovskaya et al, 2010 ).…”
Section: Introductionmentioning
confidence: 99%