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VEGFR2 signaling drives meningeal vascular regeneration upon head injury

DC Field Value Language
dc.contributor.authorKoh, B.I.-
dc.contributor.authorHyuek Jong Lee-
dc.contributor.authorPil Ae Kwak-
dc.contributor.authorMyung Jin Yang-
dc.contributor.authorKim, J.-H.-
dc.contributor.authorKim, H.-S.-
dc.contributor.authorGou Young Koh-
dc.contributor.authorKim, I.-
dc.date.accessioned2021-01-11T08:50:04Z-
dc.date.accessioned2021-01-11T08:50:04Z-
dc.date.available2021-01-11T08:50:04Z-
dc.date.available2021-01-11T08:50:04Z-
dc.date.created2020-09-09-
dc.date.issued2020-07-
dc.identifier.issn2041-1723-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/9033-
dc.description.abstractUpon severe head injury (HI), blood vessels of the meninges and brain parenchyma are inevitably damaged. While limited vascular regeneration of the injured brain has been studied extensively, our understanding of meningeal vascular regeneration following head injury is quite limited. Here, we identify key pathways governing meningeal vascular regeneration following HI. Rapid and complete vascular regeneration in the meninges is predominantly driven by VEGFR2 signaling. Substantial increase of VEGFR2 is observed in both human patients and mouse models of HI, and endothelial cell-specific deletion of Vegfr2 in the latter inhibits meningeal vascular regeneration. We further identify the facilitating, stabilizing and arresting roles of Tie2, PDGFRβ and Dll4 signaling, respectively, in meningeal vascular regeneration. Prolonged inhibition of this angiogenic process following HI compromises immunological and stromal integrity of the injured meninges. These findings establish a molecular framework for meningeal vascular regeneration after HI, and may guide development of wound healing therapeutics-
dc.description.uri1-
dc.language영어-
dc.publisherNature Publishing Group-
dc.titleVEGFR2 signaling drives meningeal vascular regeneration upon head injury-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000560401200002-
dc.identifier.scopusid2-s2.0-85088878220-
dc.identifier.rimsid72844-
dc.contributor.affiliatedAuthorHyuek Jong Lee-
dc.contributor.affiliatedAuthorPil Ae Kwak-
dc.contributor.affiliatedAuthorMyung Jin Yang-
dc.contributor.affiliatedAuthorGou Young Koh-
dc.identifier.doi10.1038/s41467-020-17545-2-
dc.identifier.bibliographicCitationNature Communications, v.11, no.1, pp.1 - 17-
dc.citation.titleNature Communications-
dc.citation.volume11-
dc.citation.number1-
dc.citation.startPage1-
dc.citation.endPage17-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalWebOfScienceCategoryMultidisciplinary Sciences-
dc.subject.keywordPlusENDOTHELIAL GROWTH-FACTOR-
dc.subject.keywordPlusTRAUMATIC BRAIN-INJURY-
dc.subject.keywordPlusANGIOGENESIS-
dc.subject.keywordPlusMACROPHAGES-
dc.subject.keywordPlusNEUROGENESIS-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusVESSELS-
dc.subject.keywordPlusMODELS-
dc.subject.keywordPlusSYSTEM-
dc.subject.keywordPlusFLUID-
dc.subject.keywordAuthorENDOTHELIAL GROWTH-FACTOR-
dc.subject.keywordAuthorTRAUMATIC BRAIN-INJURY-
dc.subject.keywordAuthorANGIOGENESIS-
dc.subject.keywordAuthorMACROPHAGES-
dc.subject.keywordAuthorNEUROGENESIS-
dc.subject.keywordAuthorSYSTEM-
dc.subject.keywordAuthorFLUID-
dc.subject.keywordAuthorMECHANISMS-
dc.subject.keywordAuthorVESSELS-
dc.subject.keywordAuthorMODELS-
Appears in Collections:
Center for Vascular Research(혈관 연구단) > 1. Journal Papers (저널논문)
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