Please use this identifier to cite or link to this item: http://dx.doi.org/10.25673/113036
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dc.contributor.authorDubourg, Virginie-
dc.contributor.authorSchwerdt, Gerald-
dc.contributor.authorSchreier, Barbara-
dc.contributor.authorKopf, Michael-
dc.contributor.authorMildenberger, Sigrid-
dc.contributor.authorBenndorf, Ralf-
dc.contributor.authorGekle, Michael-
dc.date.accessioned2024-01-15T09:29:50Z-
dc.date.available2024-01-15T09:29:50Z-
dc.date.issued2023-
dc.identifier.urihttps://opendata.uni-halle.de//handle/1981185920/114993-
dc.identifier.urihttp://dx.doi.org/10.25673/113036-
dc.description.abstractVascular smooth muscle cells (VSMC) are critical for the vascular tone, but they can also drive the development of vascular diseases when they lose their contractile phenotype and de-differentiate. Previous studies showed that the epidermal growth factor receptor (EGFR) of VSMC is critical for vascular health, but most of the underlying mechanisms by which VSMC-EGFR controls vascular fate have remained unknown. We combined RNA-sequencing and bioinformatics analysis to characterize the effect of EGFR-activation on the transcriptome of human primary VSMC (from different female donors) and to identify potentially affected cellular processes. Our results indicate that the activation of human VSMC-EGFR is sufficient to trigger a phenotypical switch toward a proliferative and inflammatory phenotype. The extent of this effect is nonetheless partly donor-dependent. Our hypothesis-generating study thus provides a first insight into mechanisms that could partly explain variable susceptibilities to vascular diseases in between individuals.eng
dc.language.isoeng-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subject.ddc610-
dc.titleTranscriptional impact of EGFR activation in human female vascular smooth muscle cellseng
dc.typeArticle-
local.versionTypepublishedVersion-
local.bibliographicCitation.journaltitleiScience-
local.bibliographicCitation.volume26-
local.bibliographicCitation.issue11-
local.bibliographicCitation.publishernameElsevier-
local.bibliographicCitation.publisherplaceAmsterdam-
local.bibliographicCitation.doi10.1016/j.isci.2023.108286-
local.openaccesstrue-
dc.identifier.ppn1873186010-
cbs.publication.displayform2023-
local.bibliographicCitation.year2023-
cbs.sru.importDate2024-01-15T09:29:17Z-
local.bibliographicCitationEnthalten in iScience - Amsterdam : Elsevier, 2018-
local.accessrights.dnbfree-
Appears in Collections:Open Access Publikationen der MLU

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