About: Double-Stranded RNA Attenuates the Barrier Function of Human Pulmonary Artery Endothelial Cells

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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	Double-Stranded RNA Attenuates the Barrier Function of Human Pulmonary Artery Endothelial Cells
Creator	Bálint, Z Konya, V Nagaraj, C Végh, A Zabini, D
Source	PMC
abstract	Circulating RNA may result from excessive cell damage or acute viral infection and can interact with vascular endothelial cells. Despite the obvious clinical implications associated with the presence of circulating RNA, its pathological effects on endothelial cells and the governing molecular mechanisms are still not fully elucidated. We analyzed the effects of double stranded RNA on primary human pulmonary artery endothelial cells (hPAECs). The effect of natural and synthetic double-stranded RNA (dsRNA) on hPAECs was investigated using trans-endothelial electric resistance, molecule trafficking, calcium (Ca(2+)) homeostasis, gene expression and proliferation studies. Furthermore, the morphology and mechanical changes of the cells caused by synthetic dsRNA was followed by in-situ atomic force microscopy, by vascular-endothelial cadherin and F-actin staining. Our results indicated that exposure of hPAECs to synthetic dsRNA led to functional deficits. This was reflected by morphological and mechanical changes and an increase in the permeability of the endothelial monolayer. hPAECs treated with synthetic dsRNA accumulated in the G1 phase of the cell cycle. Additionally, the proliferation rate of the cells in the presence of synthetic dsRNA was significantly decreased. Furthermore, we found that natural and synthetic dsRNA modulated Ca(2+) signaling in hPAECs by inhibiting the sarco-endoplasmic Ca(2+)-ATPase (SERCA) which is involved in the regulation of the intracellular Ca(2+) homeostasis and thus cell growth. Even upon synthetic dsRNA stimulation silencing of SERCA3 preserved the endothelial monolayer integrity. Our data identify novel mechanisms by which dsRNA can disrupt endothelial barrier function and these may be relevant in inflammatory processes.
has issue date	2013-06-03(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0063776
bibo:pmid	23755110
has license	cc-by
sha1sum (hex)	0b180c5c5edf329811114548e19a708303e7c1c2
schema:url	https://doi.org/10.1371/journal.pone.0063776
resource representing a document's title	Double-Stranded RNA Attenuates the Barrier Function of Human Pulmonary Artery Endothelial Cells
has PubMed Central identifier	PMC3670875
has PubMed identifier	23755110
schema:publication	PLoS One
resource representing a document's body	covid:0b180c5c5edf329811114548e19a708303e7c1c2#body_text
is schema:about of	named entity 'effects' named entity 'cell damage' named entity 'endothelial cells' named entity 'accumulated' named entity 'morphological' named entity 'dsRNA' named entity 'molecule' named entity 'Pulmonary' named entity 'HUMAN' covid:arg/0b180c5c5edf329811114548e19a708303e7c1c2 named entity 'MONOLAYER' named entity 'SYNTHETIC' named entity 'TREATED WITH' named entity 'USING' named entity 'PRESERVED' named entity 'MORPHOLOGICAL' named entity 'CELL CYCLE' named entity 'MOLECULE' named entity 'CELLS' named entity 'RESULT' named entity 'SIGNALING' named entity 'OUR' named entity 'DOUBLE STRANDED RNA' named entity 'DATA' named entity 'CLINICAL' named entity 'CAUSED BY' named entity 'ITS' named entity 'VIRAL INFECTION' named entity 'INDICATED' named entity 'LED' named entity 'GENE EXPRESSION' named entity 'ACCUMULATED' named entity 'CELL DAMAGE' named entity 'CHANGES' named entity 'EFFECTS' named entity 'MORPHOLOGY' named entity 'DEFICITS' named entity 'HUMAN' named entity 'HOMEOSTASIS' named entity 'ENDOTHELIAL' named entity 'EXPOSURE' named entity 'INTEGRITY' named entity 'DECREASED' named entity 'INVESTIGATED' named entity 'PULMONARY ARTERY' named entity 'PROCESSES' named entity 'INFLAMMATORY' named entity 'TRAFFICKING' named entity 'EXCESSIVE' named entity 'RESULTS' named entity 'BARRIER FUNCTION' named entity 'MAY BE' named entity 'DSRNA' named entity 'NOVEL' named entity 'ACUTE' named entity 'ATOMIC FORCE MICROSCOPY' named entity 'THESE' named entity 'ELECTRIC RESISTANCE' named entity 'ASSOCIATED WITH' named entity 'DISRUPT' named entity 'MECHANICAL' named entity 'INCREASE' named entity 'INTERACT' named entity 'FOLLOWED BY' named entity 'MODULATED' named entity 'PULMONARY ARTERY' named entity 'ENDOTHELIAL CELLS' named entity 'INHIBITING' named entity 'DOUBLE-STRANDED RNA' named entity 'PRIMARY' named entity 'STUDIES' named entity 'MOLECULAR' named entity 'IN-SITU' named entity 'RATE' named entity 'REFLECTED' named entity 'EFFECT' named entity 'CELL GROWTH'

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