Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression

Background: Endothelial dysfunction is implicated in various inflammatory diseases such as ischemic stroke, heart attack, organ failure, and COVID-19. Recent studies have shown that endothelial dysfunction in the brain is attributed to excessive inflammatory responses caused by the SARS-CoV-2 infect...

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Main Authors: Abhimanyu Thakur, Lifan Liang, Sourav Banerjee, Kui Zhang
Format: Article
Language:English
Published: MDPI AG 2023-05-01
Series:Brain Sciences
Subjects:
Online Access:https://www.mdpi.com/2076-3425/13/5/762
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author Abhimanyu Thakur
Lifan Liang
Sourav Banerjee
Kui Zhang
author_facet Abhimanyu Thakur
Lifan Liang
Sourav Banerjee
Kui Zhang
author_sort Abhimanyu Thakur
collection DOAJ
description Background: Endothelial dysfunction is implicated in various inflammatory diseases such as ischemic stroke, heart attack, organ failure, and COVID-19. Recent studies have shown that endothelial dysfunction in the brain is attributed to excessive inflammatory responses caused by the SARS-CoV-2 infection, leading to increased permeability of the blood-brain barrier and consequently neurological damage. Here, we aim to examine the single-cell transcriptomic landscape of endothelial dysfunction in COVID-19 and its implications for glioblastoma (GBM) progression. Methods: Single-cell transcriptome data GSE131928 and GSE159812 were obtained from the gene expression omnibus (GEO) to analyze the expression profiles of key players in innate immunity and inflammation between brain endothelial dysfunction caused by COVID-19 and GBM progression. Results: Single-cell transcriptomic analysis of the brain of COVID-19 patients revealed that endothelial cells had undergone significant transcriptomic changes, with several genes involved in immune responses and inflammation upregulated. Moreover, transcription factors were observed to modulate this inflammation, including interferon-regulated genes. Conclusions: The results indicate a significant overlap between COVID-19 and GBM in the context of endothelial dysfunction, suggesting that there may be an endothelial dysfunction link connecting severe SARS-CoV-2 infection in the brain to GBM progression.
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spelling doaj.art-bd0556407ff6409c9a20b34935a5fc5c2023-11-18T00:42:26ZengMDPI AGBrain Sciences2076-34252023-05-0113576210.3390/brainsci13050762Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma ProgressionAbhimanyu Thakur0Lifan Liang1Sourav Banerjee2Kui Zhang3Centre for Regenerative Medicine and Health, Hong Kong Institute of Science and Innovation—CAS Limited, Hong Kong 999077, ChinaDepartment of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA 15206, USADepartment of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee DD1 9SY, UKState Key Laboratory of Resource Insects, College of Sericulture, Textile and Biomass Sciences, Southwest University, Chongqing 400716, ChinaBackground: Endothelial dysfunction is implicated in various inflammatory diseases such as ischemic stroke, heart attack, organ failure, and COVID-19. Recent studies have shown that endothelial dysfunction in the brain is attributed to excessive inflammatory responses caused by the SARS-CoV-2 infection, leading to increased permeability of the blood-brain barrier and consequently neurological damage. Here, we aim to examine the single-cell transcriptomic landscape of endothelial dysfunction in COVID-19 and its implications for glioblastoma (GBM) progression. Methods: Single-cell transcriptome data GSE131928 and GSE159812 were obtained from the gene expression omnibus (GEO) to analyze the expression profiles of key players in innate immunity and inflammation between brain endothelial dysfunction caused by COVID-19 and GBM progression. Results: Single-cell transcriptomic analysis of the brain of COVID-19 patients revealed that endothelial cells had undergone significant transcriptomic changes, with several genes involved in immune responses and inflammation upregulated. Moreover, transcription factors were observed to modulate this inflammation, including interferon-regulated genes. Conclusions: The results indicate a significant overlap between COVID-19 and GBM in the context of endothelial dysfunction, suggesting that there may be an endothelial dysfunction link connecting severe SARS-CoV-2 infection in the brain to GBM progression.https://www.mdpi.com/2076-3425/13/5/762COVID-19SARS-CoV-2endothelial dysfunctionbrainsingle-cell transcriptomic
spellingShingle Abhimanyu Thakur
Lifan Liang
Sourav Banerjee
Kui Zhang
Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression
Brain Sciences
COVID-19
SARS-CoV-2
endothelial dysfunction
brain
single-cell transcriptomic
title Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression
title_full Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression
title_fullStr Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression
title_full_unstemmed Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression
title_short Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression
title_sort single cell transcriptomics reveals evidence of endothelial dysfunction in the brains of covid 19 patients with implications for glioblastoma progression
topic COVID-19
SARS-CoV-2
endothelial dysfunction
brain
single-cell transcriptomic
url https://www.mdpi.com/2076-3425/13/5/762
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