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The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood–brain barrier

Authors
  • Buzhdygan, Tetyana P.1, 2
  • DeOre, Brandon J.3
  • Baldwin-Leclair, Abigail3
  • Bullock, Trent A.1, 2
  • McGary, Hannah M.1
  • Khan, Jana A.1
  • Razmpour, Roshanak1
  • Hale, Jonathan F.1
  • Galie, Peter A.3
  • Potula, Raghava1, 2
  • Andrews, Allison M.1, 2
  • Ramirez, Servio H.1, 2, 4
  • 1 Department of Pathology and Laboratory Medicine, The Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States of America
  • 2 Center for Substance Abuse Research, The Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, United States of America
  • 3 Department of Biomedical Engineering, Rowan University, Glassboro, NJ 08028, United States of America
  • 4 The Shriners Hospitals Pediatric Research Center, Philadelphia, PA 19140, United States of America
Type
Published Article
Journal
Neurobiology of Disease
Publisher
Elsevier
Publication Date
Oct 11, 2020
Volume
146
Pages
105131–105131
Identifiers
DOI: 10.1016/j.nbd.2020.105131
PMID: 33053430
PMCID: PMC7547916
Source
PubMed Central
Keywords
License
Unknown

Abstract

• SARS-CoV-2 is known to bind to ACE2. ACE2 is upregulated in the human brain vasculature of hypertensive and dementia cases. • The SARS-CoV-2 spike protein does not acutely affect the viability of brain endothelial cells. • Blood-brain barrier function is negatively affected by SARS-CoV-2 spike protein subunits. • Brain endothelial cells show a distinct pro-inflammatory response when exposed to various SARS-CoV-2 spike protein subunits. • Mechanistically, barrier disruption may be explained by induction of members of the MMP family of proteins.

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