000128991 001__ 128991
000128991 005__ 20210129211209.0
000128991 0247_ $$2doi$$a10.1093/gerona/gls242
000128991 0247_ $$2pmid$$apmid:23239824
000128991 0247_ $$2ISSN$$a1758-535X
000128991 0247_ $$2ISSN$$a1079-5006
000128991 0247_ $$2WOS$$aWOS:000322298700001
000128991 037__ $$aFZJ-2013-00514
000128991 041__ $$aENG
000128991 082__ $$a610
000128991 1001_ $$aUngvari, Z.$$b0$$eCorresponding author
000128991 245__ $$aAging-Induced Dysregulation of Dicer1-Dependent MicroRNA Expression Impairs Angiogenic Capacity of Rat Cerebromicrovascular Endothelial Cells.
000128991 260__ $$aOxford [u.a.]$$bOxford Univ. Pr.$$c2013
000128991 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1375174653_30739
000128991 3367_ $$2DataCite$$aOutput Types/Journal article
000128991 3367_ $$00$$2EndNote$$aJournal Article
000128991 3367_ $$2BibTeX$$aARTICLE
000128991 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000128991 3367_ $$2DRIVER$$aarticle
000128991 500__ $$3POF3_Assignment on 2016-02-29
000128991 520__ $$aAge-related impairment of angiogenesis is likely to play a central role in cerebromicrovascular rarefaction and development of vascular cognitive impairment, but the underlying mechanisms remain elusive. To test the hypothesis that dysregulation of Dicer1 (ribonuclease III, a key enzyme of the microRNA [miRNA] machinery) impairs endothelial angiogenic capacity in aging, primary cerebromicrovascular endothelial cells (CMVECs) were isolated from young (3 months old) and aged (24 months old) Fischer 344 × Brown Norway rats. We found an age-related downregulation of Dicer1 expression both in CMVECs and in small cerebral vessels isolated from aged rats. In aged CMVECs, Dicer1 expression was increased by treatment with polyethylene glycol-catalase. Compared with young cells, aged CMVECs exhibited altered miRNA expression profile, which was associated with impaired proliferation, adhesion to vitronectin, collagen and fibronectin, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing technology), and impaired ability to form capillary-like structures. Overexpression of Dicer1 in aged CMVECs partially restored miRNA expression profile and significantly improved angiogenic processes. In young CMVECs, downregulation of Dicer1 (siRNA) resulted in altered miRNA expression profile associated with impaired proliferation, adhesion, migration, and tube formation, mimicking the aging phenotype. Collectively, we found that Dicer1 is essential for normal endothelial angiogenic processes, suggesting that age-related dysregulation of Dicer1-dependent miRNA expression may be a potential mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging.
000128991 536__ $$0G:(DE-HGF)POF2-452$$a452 - Structural Biology (POF2-452)$$cPOF2-452$$fPOF II$$x0
000128991 588__ $$aDataset connected to
000128991 7001_ $$0P:(DE-HGF)0$$aTucsek, Zsuzsanna$$b1
000128991 7001_ $$0P:(DE-HGF)0$$aSosnowska, Danuta$$b2
000128991 7001_ $$0P:(DE-HGF)0$$aToth, Peter$$b3
000128991 7001_ $$0P:(DE-HGF)0$$aGautam, Tripti$$b4
000128991 7001_ $$0P:(DE-HGF)0$$aPodlutsky, Andrej$$b5
000128991 7001_ $$0P:(DE-Juel1)128805$$aCsiszar, Agnes$$b6
000128991 7001_ $$0P:(DE-HGF)0$$aLosonczy, Gyorgy$$b7
000128991 7001_ $$0P:(DE-HGF)0$$aValcarcel-Ares, M Noa$$b8
000128991 7001_ $$0P:(DE-HGF)0$$aSonntag, William E$$b9
000128991 7001_ $$0P:(DE-HGF)0$$aCsiszar, Anna$$b10
000128991 773__ $$0PERI:(DE-600)2043927-1$$a10.1093/gerona/gls242$$gp. gls242$$n8$$p877-891$$tThe @journals of gerontology / A$$v68$$x1758-535X$$y2013
000128991 8564_ $$uhttps://juser.fz-juelich.de/record/128991/files/FZJ-2013-00514.pdf$$yRestricted$$zPublished final document.
000128991 909CO $$ooai:juser.fz-juelich.de:128991$$pVDB
000128991 9141_ $$y2013
000128991 915__ $$0StatID:(DE-HGF)0040$$2StatID$$aPeer review unknown
000128991 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR
000128991 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000128991 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000128991 915__ $$0StatID:(DE-HGF)0130$$2StatID$$aWoS$$bSocial Sciences Citation Index
000128991 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000128991 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000128991 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000128991 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000128991 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000128991 915__ $$0StatID:(DE-HGF)0400$$2StatID$$aAllianz-Lizenz / DFG
000128991 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz
000128991 915__ $$0StatID:(DE-HGF)1020$$2StatID$$aDBCoverage$$bCurrent Contents - Social and Behavioral Sciences
000128991 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000128991 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)128805$$aForschungszentrum Jülich GmbH$$b6$$kFZJ
000128991 9132_ $$0G:(DE-HGF)POF3-559H$$1G:(DE-HGF)POF3-550$$2G:(DE-HGF)POF3-500$$aDE-HGF$$bKey Technologies$$lBioSoft – Fundamentals for future Technologies in the fields of Soft Matter and Life Sciences$$vAddenda$$x0
000128991 9131_ $$0G:(DE-HGF)POF2-452$$1G:(DE-HGF)POF2-450$$2G:(DE-HGF)POF2-400$$3G:(DE-HGF)POF2$$4G:(DE-HGF)POF$$aDE-HGF$$bSchlüsseltechnologien$$lBioSoft$$vStructural Biology$$x0
000128991 920__ $$lyes
000128991 9201_ $$0I:(DE-Juel1)ICS-7-20110106$$kICS-7$$lBiomechanik$$x0
000128991 980__ $$ajournal
000128991 980__ $$aVDB
000128991 980__ $$aUNRESTRICTED
000128991 980__ $$aI:(DE-Juel1)ICS-7-20110106
000128991 981__ $$aI:(DE-Juel1)IBI-2-20200312