Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8143
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dc.contributor.authorZehendner, Christoph M.-
dc.contributor.authorWedler, Hannah E.-
dc.contributor.authorLuhmann, Heiko-
dc.date.accessioned2022-10-21T08:05:24Z-
dc.date.available2022-10-21T08:05:24Z-
dc.date.issued2013-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/8158-
dc.description.abstractCortical function is impaired in various disorders of the central nervous system including Alzheimer's disease, autism and schizophrenia. Some of these disorders are speculated to be associated with insults in early brain development. Pericytes have been shown to regulate neurovascular integrity in development, health and disease. Hence, precisely controlled mechanisms must have evolved in evolution to operate pericyte proliferation, repair and cell fate within the neurovascular unit (NVU). It is well established that pericyte deficiency leads to NVU injury resulting in cognitive decline and neuroinflammation in cortical layers. However, little is known about the role of pericytes in pathophysiological processes of the developing cortex. Here we introduce an in vitro model that enables to precisely study pericytes in the immature cortex and show that moderate inflammation and hypoxia result in caspase-3 mediated pericyte loss. Using heterozygous EYFP-NG2 mouse mutants we performed live imaging of pericytes for several days in vitro. In addition we show that pericytes maintain their capacity to proliferate which may allow cell-based therapies like reprogramming of pericytes into induced neuronal cells in the presented approach.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleA novel in vitro model to study pericytes in the neurovascular unit of the developing cortexen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-8143-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titlePLoS onede
jgu.journal.volume8de
jgu.journal.issue11de
jgu.pages.alternativee81637de
jgu.publisher.year2013-
jgu.publisher.namePLoSde
jgu.publisher.placeLawrence, Kan.de
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0081637de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.identifier.pmid24278454-
jgu.subject.ddccode610de
opus.date.modified2018-08-02T09:59:26Z-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Institut für Physiologie und Pathophysiologiede_DE
opus.identifier.opusid25276-
opus.importsourcepubmed-
opus.institute.number0403-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedZehendner, Christoph M.-
opus.affiliatedLuhmann, Heiko-
jgu.publisher.doi10.1371/journal.pone.0081637de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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