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10.3390/v14050891

http://scihub22266oqcxt.onion/10.3390/v14050891
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35632633!9143673!35632633
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suck abstract from ncbi


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pmid35632633      Viruses 2022 ; 14 (5): ä
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  • Molecular Cross-Talk between Integrins and Cadherins Leads to a Loss of Vascular Barrier Integrity during SARS-CoV-2 Infection #MMPMID35632633
  • Nader D; Kerrigan SW
  • Viruses 2022[Apr]; 14 (5): ä PMID35632633show ga
  • The vascular barrier is heavily injured following SARS-CoV-2 infection and contributes enormously to life-threatening complications in COVID-19. This endothelial dysfunction is associated with the phlogistic phenomenon of cytokine storms, thrombotic complications, abnormal coagulation, hypoxemia, and multiple organ failure. The mechanisms surrounding COVID-19 associated endotheliitis have been widely attributed to ACE2-mediated pathways. However, integrins are emerging as possible receptor candidates for SARS-CoV-2, and their complex intracellular signaling events are essential for maintaining endothelial homeostasis. Here, we showed that the spike protein of SARS-CoV-2 depends on its RGD motif to drive barrier dysregulation by hijacking integrin alphaVbeta3, expressed on human endothelial cells. This triggers the redistribution and internalization of major junction protein VE-Cadherin which leads to the barrier disruption phenotype. Both extracellular and intracellular inhibitors of integrin alphaVbeta3 prevented these effects, similarly to the RGD-cyclic peptide compound Cilengitide, which suggests that the spike protein-through its RGD motif-binds to alphaVbeta3 and elicits vascular leakage events. These findings support integrins as an additional receptor for SARS-CoV-2, particularly as integrin engagement can elucidate many of the adverse endothelial dysfunction events that stem from COVID-19.
  • |*COVID-19[MESH]
  • |*Spike Glycoprotein, Coronavirus/metabolism[MESH]
  • |Cadherins[MESH]
  • |Endothelial Cells/metabolism[MESH]
  • |Humans[MESH]
  • |Integrin alphaVbeta3[MESH]


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