LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 2 of total 2

Search options

  1. Article: SARS-CoV-2 Structural Proteins Exposure Alter Thrombotic and Inflammatory Responses in Human Endothelial Cells.

    Freda, Christopher Thor / Yin, Wei / Ghebrehiwet, Berhane / Rubenstein, David A

    Cellular and molecular bioengineering

    2021  Volume 15, Issue 1, Page(s) 43–53

    Abstract: Introduction: We have experienced a pandemic induced by the interaction of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) structural proteins with innate structures. These interactions are especially prevalent for patients with underlying ... ...

    Abstract Introduction: We have experienced a pandemic induced by the interaction of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) structural proteins with innate structures. These interactions are especially prevalent for patients with underlying pathologies, such as cardiovascular diseases. However, there has been limited work to uncover the range of responses induced by SARS-CoV-2 structural proteins. Thus, our objective was to investigate how endothelial cell pro-thrombotic and pro-inflammatory responses are altered after exposure to SARS-CoV-2 spike, nucleocapsid, and membrane-envelope proteins. We hypothesized that after a short duration exposure, endothelial cells would have a heightened thrombotic and inflammatory potential. With longer exposures, this may lead to altered disease progression and the observed increased mortality and morbidity rates in patients with underlying vascular pathologies.
    Methods: To test this hypothesis, human endothelial cells were exposed to SARS-CoV-2 structural proteins. After the exposure, the expression of thrombomodulin, PECAM-1, connexin-43, and gC1qR were assessed. In parallel, standard cell culture readouts were assessed to determine if these incubations altered cell growth and metabolism.
    Results and conclusions: We observed significant increases in thrombotic and inflammatory marker expression, with no change to the cell culture parameters (with the exception of a reduction in cell density in response to one SARS-CoV-2 structural protein). Importantly, these observations were dependent on the viral structural protein the cells were exposed to, suggesting that the interactions of SARS-CoV-2 with innate cells is complex and must be uncovered. Combined, this suggests that SARS-CoV-2 structural proteins can regulate inflammatory and thrombotic responses that underlie common pathologies observed during COVID-19.
    Language English
    Publishing date 2021-08-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2416037-4
    ISSN 1865-5033 ; 1865-5025
    ISSN (online) 1865-5033
    ISSN 1865-5025
    DOI 10.1007/s12195-021-00696-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts.

    Freda, Christopher Thor / Yin, Wei / Ghebrehiwet, Berhane / Rubenstein, David A

    Clinical immunology (Orlando, Fla.)

    2021  Volume 227, Page(s) 108733

    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for many pathological processes, including altered vascular disease development, dysfunctional thrombosis and a heightened inflammatory response. However, there is limited work ... ...

    Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for many pathological processes, including altered vascular disease development, dysfunctional thrombosis and a heightened inflammatory response. However, there is limited work to determine the underlying cellular responses induced by exposure to SARS-CoV-2 structural proteins. Thus, our objective was to investigate how human arterial adventitial fibroblasts inflammation, thrombosis and diabetic disease markers are altered in response to Spike, Nucleocapsid and Membrane-Envelope proteins. We hypothesized that after a short-term exposure to SARS-CoV-2 proteins, adventitial fibroblasts would have a higher expression of inflammatory, thrombotic and diabetic proteins, which would support a mechanism for altered vascular disease progression. After incubation, the expression of gC1qR, ICAM-1, tissue factor, RAGE and GLUT-4 was significantly up-regulated. In general, the extent of expression was different for each SARS-CoV-2 protein, suggesting that SARS-CoV-2 proteins interact with cells through different mechanisms. Thus, SARS-CoV-2 protein interaction with vascular cells may regulate vascular disease responses.
    MeSH term(s) Aorta/cytology ; Aorta/metabolism ; COVID-19/immunology ; Cardiovascular Diseases/complications ; Cardiovascular Diseases/immunology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/virology ; Carrier Proteins/metabolism ; Cell Survival/immunology ; Cell Survival/physiology ; Complement System Proteins/immunology ; Coronavirus Envelope Proteins/immunology ; Coronavirus Nucleocapsid Proteins/immunology ; Coronavirus Nucleocapsid Proteins/metabolism ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/virology ; Fibroblasts/metabolism ; Glucose Transporter Type 4/metabolism ; Humans ; Inflammation/metabolism ; Inflammation/virology ; Intercellular Adhesion Molecule-1/metabolism ; Mitochondrial Proteins/metabolism ; Receptor for Advanced Glycation End Products/metabolism ; SARS-CoV-2/immunology ; Spike Glycoprotein, Coronavirus/immunology ; Thrombosis/complications ; Thrombosis/metabolism ; Thrombosis/virology
    Chemical Substances AGER protein, human ; C1QBP protein, human ; Carrier Proteins ; Coronavirus Envelope Proteins ; Coronavirus Nucleocapsid Proteins ; Glucose Transporter Type 4 ; ICAM1 protein, human ; Mitochondrial Proteins ; Receptor for Advanced Glycation End Products ; SLC2A4 protein, human ; Spike Glycoprotein, Coronavirus ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2021-04-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2021.108733
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top