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  1. Article ; Online: Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants.

    Wagner, Julian U G / Bojkova, Denisa / Shumliakivska, Mariana / Luxán, Guillermo / Nicin, Luka / Aslan, Galip S / Milting, Hendrik / Kandler, Joshua D / Dendorfer, Andreas / Heumueller, Andreas W / Fleming, Ingrid / Bibli, Sofia-Iris / Jakobi, Tobias / Dieterich, Christoph / Zeiher, Andreas M / Ciesek, Sandra / Cinatl, Jindrich / Dimmeler, Stefanie

    Basic research in cardiology

    2021  Volume 116, Issue 1, Page(s) 42

    Abstract: ... whether different types of endothelial cells are susceptible to SARS-CoV-2. Human endothelial cells from different ... in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 ... ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B.1.1.7, B.1.351, and P.2 ...

    Abstract Coronavirus disease 2019 (COVID-19) spawned a global health crisis in late 2019 and is caused by the novel coronavirus SARS-CoV-2. SARS-CoV-2 infection can lead to elevated markers of endothelial dysfunction associated with higher risk of mortality. It is unclear whether endothelial dysfunction is caused by direct infection of endothelial cells or is mainly secondary to inflammation. Here, we investigate whether different types of endothelial cells are susceptible to SARS-CoV-2. Human endothelial cells from different vascular beds including umbilical vein endothelial cells, coronary artery endothelial cells (HCAEC), cardiac and lung microvascular endothelial cells, or pulmonary arterial cells were inoculated in vitro with SARS-CoV-2. Viral spike protein was only detected in HCAECs after SARS-CoV-2 infection but not in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B.1.1.7, B.1.351, and P.2 resulted in significantly higher levels of viral spike protein. Despite this, no intracellular double-stranded viral RNA was detected and the supernatant did not contain infectious virus. Analysis of the cellular distribution of the spike protein revealed that it co-localized with endosomal calnexin. SARS-CoV-2 infection did induce the ER stress gene EDEM1, which is responsible for clearance of misfolded proteins from the ER. Whereas the wild type of SARS-CoV-2 did not induce cytotoxic or pro-inflammatory effects, the variant B.1.1.7 reduced the HCAEC cell number. Of the different tested endothelial cells, HCAECs showed highest viral uptake but did not promote virus replication. Effects on cell number were only observed after infection with the variant B.1.1.7, suggesting that endothelial protection may be particularly important in patients infected with this variant.
    MeSH term(s) Angiotensin-Converting Enzyme 2/metabolism ; Calnexin/metabolism ; Cells, Cultured ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/virology ; Endoplasmic Reticulum Stress ; Endothelial Cells/metabolism ; Endothelial Cells/virology ; Host-Pathogen Interactions ; Humans ; Membrane Proteins/metabolism ; Receptors, Virus/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism ; SARS-CoV-2/pathogenicity ; Spike Glycoprotein, Coronavirus/metabolism
    Chemical Substances CANX protein, human ; EDEM1 protein, human ; Membrane Proteins ; Receptors, Virus ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Calnexin (139873-08-8) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Language English
    Publishing date 2021-07-05
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-021-00882-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants

    Wagner, J.U.G. / Bojkova, D. / Shumliakivska, M. / Luxan, G. / Nicin, L. / Aslan, G.S. / Milting, H. / Kandler, J.D. / Dendorfer, A. / Heumueller, A.W. / Fleming, I. / Bibli, S.-I. / Jakobi, T. / Dieterich, C. / Zeiher, A.M. / Ciesek, S. / Cinatl, J. / Dimmeler, S.

    2021  

    Abstract: ... we investigate whether different types of endothelial cells are susceptible to SARS-CoV-2. Human ... infection but not in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 ... receptor angiotensin-converting enzyme 2 (ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B ...

    Abstract Art. 42, 12 S.

    Coronavirus disease 2019 (COVID-19) spawned a global health crisis in late 2019 and is caused by the novel coronavirus SARS-CoV-2. SARS-CoV-2 infection can lead to elevated markers of endothelial dysfunction associated with higher risk of mortality. It is unclear whether endothelial dysfunction is caused by direct infection of endothelial cells or is mainly secondary to inflammation. Here, we investigate whether different types of endothelial cells are susceptible to SARS-CoV-2. Human endothelial cells from different vascular beds including umbilical vein endothelial cells, coronary artery endothelial cells (HCAEC), cardiac and lung microvascular endothelial cells, or pulmonary arterial cells were inoculated in vitro with SARS-CoV-2. Viral spike protein was only detected in HCAECs after SARS-CoV-2 infection but not in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B.1.1.7, B.1.351, and P.2 resulted in significantly higher levels of viral spike protein. Despite this, no intracellular double-stranded viral RNA was detected and the supernatant did not contain infectious virus. Analysis of the cellular distribution of the spike protein revealed that it co-localized with endosomal calnexin. SARS-CoV-2 infection did induce the ER stress gene EDEM1, which is responsible for clearance of misfolded proteins from the ER. Whereas the wild type of SARS-CoV-2 did not induce cytotoxic or pro-inflammatory effects, the variant B.1.1.7 reduced the HCAEC cell number. Of the different tested endothelial cells, HCAECs showed highest viral uptake but did not promote virus replication. Effects on cell number were only observed after infection with the variant B.1.1.7, suggesting that endothelial protection may be particularly important in patients infected with this variant.

    116

    Nr.1
    Keywords 540 ; 616 ; 571 ; 572
    Subject code 570
    Language English
    Publishing country de
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Smoking-Mediated Upregulation of the Androgen Pathway Leads to Increased SARS-CoV-2 Susceptibility.

    Chakladar, Jaideep / Shende, Neil / Li, Wei Tse / Rajasekaran, Mahadevan / Chang, Eric Y / Ongkeko, Weg M

    International journal of molecular sciences

    2020  Volume 21, Issue 10

    Abstract: ... protease necessary for SARS-CoV-2 entry into host cells, ACE2 and TMPRSS2, respectively, were upregulated ... smoking may affect the SARS-CoV-2 infection rate. We analyzed sequencing data from lung and oral ... pathway regulatory genes. These data provide a potential model for the increased susceptibility of smoking ...

    Abstract The COVID-19 pandemic is marked by a wide range of clinical disease courses, ranging from asymptomatic to deadly. There have been many studies seeking to explore the correlations between COVID-19 clinical outcomes and various clinical variables, including age, sex, race, underlying medical problems, and social habits. In particular, the relationship between smoking and COVID-19 outcome is controversial, with multiple conflicting reports in the current literature. In this study, we aim to analyze how smoking may affect the SARS-CoV-2 infection rate. We analyzed sequencing data from lung and oral epithelial samples obtained from The Cancer Genome Atlas (TCGA). We found that the receptor and transmembrane protease necessary for SARS-CoV-2 entry into host cells, ACE2 and TMPRSS2, respectively, were upregulated in smoking samples from both lung and oral epithelial tissue. We then explored the mechanistic hypothesis that smoking may upregulate ACE2 expression through the upregulation of the androgen pathway. ACE2 and TMPRSS2 upregulation were both correlated to androgen pathway enrichment and the specific upregulation of central pathway regulatory genes. These data provide a potential model for the increased susceptibility of smoking patients to COVID-19 and encourage further exploration into the androgen and tobacco upregulation of ACE2 to understand the potential clinical ramifications.
    MeSH term(s) Alveolar Epithelial Cells/metabolism ; Androgens/metabolism ; Angiotensin-Converting Enzyme 2 ; COVID-19 ; Coronavirus Infections/epidemiology ; Coronavirus Infections/genetics ; Coronavirus Infections/metabolism ; Humans ; Mouth Mucosa/metabolism ; Pandemics ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/genetics ; Pneumonia, Viral/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism ; Smoking/epidemiology ; Smoking/genetics ; Smoking/metabolism ; Up-Regulation
    Chemical Substances Androgens ; Receptors, Androgen ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Serine Endopeptidases (EC 3.4.21.-) ; TMPRSS2 protein, human (EC 3.4.21.-)
    Keywords covid19
    Language English
    Publishing date 2020-05-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21103627
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants

    Luxán, Guillermo / Dimmeler, Stefanie

    http://lobid.org/resources/99370671625606441#!, 116(1):42

    2021  

    Abstract: ... whether different types of endothelial cells are susceptible to SARS-CoV-2. Human endothelial cells from different ... in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 ... ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B.1.1.7, B.1.351, and P.2 ...

    Abstract Coronavirus disease 2019 (COVID-19) spawned a global health crisis in late 2019 and is caused by the novel coronavirus SARS-CoV-2. SARS-CoV-2 infection can lead to elevated markers of endothelial dysfunction associated with higher risk of mortality. It is unclear whether endothelial dysfunction is caused by direct infection of endothelial cells or is mainly secondary to inflammation. Here, we investigate whether different types of endothelial cells are susceptible to SARS-CoV-2. Human endothelial cells from different vascular beds including umbilical vein endothelial cells, coronary artery endothelial cells (HCAEC), cardiac and lung microvascular endothelial cells, or pulmonary arterial cells were inoculated in vitro with SARS-CoV-2. Viral spike protein was only detected in HCAECs after SARS-CoV-2 infection but not in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B.1.1.7, B.1.351, and P.2 resulted in significantly higher levels of viral spike protein. Despite this, no intracellular double-stranded viral RNA was detected and the supernatant did not contain infectious virus. Analysis of the cellular distribution of the spike protein revealed that it co-localized with endosomal calnexin. SARS-CoV-2 infection did induce the ER stress gene EDEM1, which is responsible for clearance of misfolded proteins from the ER. Whereas the wild type of SARS-CoV-2 did not induce cytotoxic or pro-inflammatory effects, the variant B.1.1.7 reduced the HCAEC cell number. Of the different tested endothelial cells, HCAECs showed highest viral uptake but did not promote virus replication. Effects on cell number were only observed after infection with the variant B.1.1.7, suggesting that endothelial protection may be particularly important in patients infected with this variant.
    Keywords Calnexin/metabolism [MeSH] ; Cells, Cultured [MeSH] ; Angiotensin-Converting Enzyme 2/metabolism [MeSH] ; ER stress ; Endoplasmic Reticulum Stress [MeSH] ; Endoplasmic Reticulum/metabolism [MeSH] ; Endoplasmic Reticulum/virology [MeSH] ; Endothelial Cells/metabolism [MeSH] ; Endothelial Cells/virology [MeSH] ; Endothelial cells ; Host-Pathogen Interactions [MeSH] ; Humans [MeSH] ; Original Contribution ; Membrane Proteins/metabolism [MeSH] ; SARS-CoV-2 ; SARS-CoV-2/genetics [MeSH] ; SARS-CoV-2/metabolism [MeSH] ; SARS-CoV-2/pathogenicity [MeSH] ; Spike Glycoprotein, Coronavirus/metabolism [MeSH] ; Receptors, Virus/metabolism [MeSH] ; Virus trapping
    Language English
    Document type Article
    Database Repository for Life Sciences

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