ArticleFluids and barriers of the CNS2024
SARS-CoV-2 causes dysfunction in human iPSC-derived brain microvascular endothelial cells potentially by modulating the Wnt signaling pathway.
Article in Fluids and barriers of the CNS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 17 citations in OpenAlex.
- SARS-CoV-2 nucleocapsid induces hyperinflammation and vascular leakage through the Toll-like receptor signaling axis in macrophages.Science advances · 2026Article
- Neurodegenerative and Cognitive Consequences of Long COVID.International journal of molecular sciences · 2026Review
- A systematic review and meta-analysis of the relationship between neuroinflammation and blood-brain barrier based onBiochemistry and biophysics reports · 2026Review
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Pathogenic breaches: how viruses compromise blood-tissue barriers.Tissue barriers · 2026Review
- Viral Infection and the Blood-Brain Barrier: Molecular Research Insights and Therapies.The Journal of infectious diseases · 2025Review
- Stem cell-derived brain-like endothelial cells to interrogateVirulence · 2025Article
- Old World alphaviruses use distinct mechanisms to infect brain microvascular endothelial cells for neuroinvasion.Cell reports · 2025Article
- SARS-CoV-2 Infection Influences Wnt/β-Catenin Pathway Components in Astrocytes.Pathogens (Basel, Switzerland) · 2025Article
- Innate immune sensors and regulators at the blood brain barrier: focus on toll-like receptors and inflammasomes as mediators of neuro-immune crosstalk and inflammation.Journal of neuroinflammation · 2025Review
- A data-mining analysis of host solute carrier family proteins in SARS-CoV-2 infection with reference to brain endothelial cells and the blood-brain barrier in COVID-19.Frontiers in neurology · 2025Article
- SARS-CoV-2 infection in microglia and its sequelae: What do we know so far?Brain, behavior, & immunity - health · 2024Review
- Compromised endothelial Wnt/β-catenin signaling mediates the blood-brain barrier disruption and leads to neuroinflammation in endotoxemia.Journal of neuroinflammation · 2024Article
- Long-term gastrointestinal symptoms and sleep quality sequelae in adolescents after COVID-19: a retrospective study.Frontiers in public health · 2024Article
- Opportunistic infections changed before and after SARS-CoV-2 infection in inflammatory bowel disease patients: a retrospective single-center study in China.Frontiers in medicine · 2024Article
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10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which is associated with various neurological symptoms, including nausea, dizziness, headache, encephalitis, and epileptic seizures. SARS-CoV-2 is considered to affect the central nervous system (CNS) by interacting with the blood-brain barrier (BBB), which is defined by tight junctions that seal paracellular gaps between brain microvascular endothelial cells (BMECs). Although SARS-CoV-2 infection of BMECs has been reported, the detailed mechanism has not been fully elucidated.
methodsUsing the original strain of SARS-CoV-2, the infection in BMECs was confirmed by a detection of intracellular RNA copy number and localization of viral particles. BMEC functions were evaluated by measuring transendothelial electrical resistance (TEER), which evaluates the integrity of tight junction dynamics, and expression levels of proinflammatory genes. BMEC signaling pathway was examined by comprehensive RNA-seq analysis.
resultsWe observed that iPSC derived brain microvascular endothelial like cells (iPSC-BMELCs) were infected with SARS-CoV-2. SARS-CoV-2 infection resulted in decreased TEER. In addition, SARS-CoV-2 infection decreased expression levels of tight junction markers CLDN3 and CLDN11. SARS-CoV-2 infection also increased expression levels of proinflammatory genes, which are known to be elevated in patients with COVID-19. Furthermore, RNA-seq analysis revealed that SARS-CoV-2 dysregulated the canonical Wnt signaling pathway in iPSC-BMELCs. Modulation of the Wnt signaling by CHIR99021 partially inhibited the infection and the subsequent inflammatory responses.
conclusionThese findings suggest that SARS-CoV-2 infection causes BBB dysfunction via Wnt signaling. Thus, iPSC-BMELCs are a useful in vitro model for elucidating COVID-19 neuropathology and drug development.
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