About: Long-Term Maintenance of the Functional Changes Induced by Influenza A Virus and/or LPS in Human Endothelial ECV-304 Cell Sublines

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About: Long-Term Maintenance of the Functional Changes Induced by Influenza A Virus and/or LPS in Human Endothelial ECV-304 Cell Sublines Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Long-Term Maintenance of the Functional Changes Induced by Influenza A Virus and/or LPS in Human Endothelial ECV-304 Cell Sublines
Creator	Sivak, K Pisareva, M Smirnova, S Smirnova, T Vorobiev, K
Source	PMC
abstract	Influenza A virus and secondary bacterial infection may have remote effects in the form of cardiovascular complications or fibrosis in different organs. However, the mechanisms governing the development of complications remain poorly studied. The present work reports the comparative assessment of the functional changes which take place in human ECV-304 endothelial cell sublines obtained previously by the long-term culturing of cells after exposure to varying infectious doses (IDs) of influenza A virus, and/or bacterial lipopolysaccharide (LPS). It has been demonstrated that, in the course of long-term culturing (six passages) after exposure to pathogenic agents (influenza virus and/or LPS), endothelial cells maintain changes in their migratory activity, permeability, and expression of mRNA for cytokines TNFα and TGFβ (along with the changes in their proliferation activity, which has been demonstrated earlier). The pattern of changes depended on the type of the agent (agents) to which the cells were exposed. The differences in migratory activity (which was at its maximum 4 h after wounding) between the cell sublines at the sixth passage correlated with the differences in their proliferation activity at the first passage (proliferation data were obtained previously). In particular, an increase in migration and proliferation was observed in the sublines exposed to low virus doses (ECV-1ID), as well as exposed to LPS (ECV-LPS), while the suppression of migration and proliferation was observed in the subline exposed to high virus doses (ECV-1000ID). In the ECV-1ID, ECV-LPS, and most notably in ECV-1ID + LPS sublines, we detected an increase in the expression of mRNA for cytokines TNFα and TGFβ, which, however, didn’t lead to the induction of apoptosis. We have also demonstrated an increase in cell permeability in the analyzed sublines, which was indicated by a decrease in the expression of the mRNAs for the genes encoding occludin and ZO-1, the tight junctions proteins . This paper also reports an evaluation of the effects of the antiviral preparations rimantadine and alpisarin on the functional state of cell sublines. As a result, it has been demonstrated that these drugs may be able to prevent the development of the pathological changes caused by influenza A virus and/or LPS in endothelial cells. The results obtained in the present work may be of use when studying the mechanisms of development of the influenza A virus and secondary bacterial infection complications.
has issue date	2019-08-26(xsd:dateTime)
bibo:doi	10.1134/s1990519x19040084
bibo:pmid	32288938
has license	no-cc
sha1sum (hex)	d881769ce120296d1b47e6b4f4e8338a17978b4d
schema:url	https://doi.org/10.1134/s1990519x19040084
resource representing a document's title	Long-Term Maintenance of the Functional Changes Induced by Influenza A Virus and/or LPS in Human Endothelial ECV-304 Cell Sublines
has PubMed Central identifier	PMC7101551
has PubMed identifier	32288938
schema:publication	Cell tissue biol
resource representing a document's body	covid:d881769ce120296d1b47e6b4f4e8338a17978b4d#body_text
is schema:about of	named entity 'doses' named entity 'high' named entity 'agent' named entity 'cells' named entity 'TNFα' named entity 'rimantadine' named entity 'exposed' named entity 'influenza A virus' named entity 'activity' named entity 'mechanisms' named entity 'induction' named entity 'demonstrated' named entity 'Author' named entity 'SECONDARY BACTERIAL INFECTION ' named entity 'DEMONSTRATED' named entity 'DRUGS' named entity 'VIRUS' named entity 'FIBROSIS' named entity 'USE' named entity 'MIGRATORY' named entity 'EFFECTS' named entity 'WOUNDING' named entity 'INFECTIOUS' named entity 'CELL PERMEABILITY' named entity 'LIPOPOLYSACCHARIDE' named entity 'COMPLICATIONS' named entity 'EXPOSURE TO' named entity 'ENDOTHELIAL CELLS' named entity 'TYPE' named entity 'LPS' named entity 'CYTOKINES' named entity 'ECV' named entity 'passage' named entity 'complications' named entity 'functional' named entity 'complications' named entity 'cell' named entity 'cardiovascular' named entity 'proliferation' named entity 'doses' named entity 'proliferation' named entity 'demonstrated' named entity 'doses' named entity 'lipopolysaccharide' named entity 'data' named entity 'LPS' named entity 'antiviral' named entity 'secondary bacterial infection' named entity 'endothelial cells' named entity 'occludin' named entity 'TGFβ' named entity 'virus' named entity 'fibrosis' named entity 'influenza A virus' named entity 'endothelial cell' named entity 'mRNAs' named entity 'LPS' named entity 'pathological states' named entity 'Rimantadine' named entity 'rimantadine' named entity 'influenza infection' named entity 'ROS' named entity 'primers' named entity 'antivirals' named entity 'expression levels' named entity 'growth factor' named entity 'mRNA' named entity 'permeability' named entity 'mRNA expression' named entity 'TNFα' named entity 'Expression levels' named entity 'virus' named entity 'microtubules' named entity 'endothelium' named entity 'mRNA' named entity 'oncogenesis' named entity 'cytokines'

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