Essential role of MALAT1 in reducing traumatic brain injury

As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of...
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Autor*in:	Na Wu [verfasserIn] Chong-Jie Cheng [verfasserIn] Jian-Jun Zhong [verfasserIn] Jun-Chi He [verfasserIn] Zhao-Si Zhang [verfasserIn] Zhi-Gang Wang [verfasserIn] Xiao-Chuan Sun [verfasserIn] Han Liu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling

Übergeordnetes Werk:	In: Neural Regeneration Research - Wolters Kluwer Medknow Publications, 2014, 17(2022), 8, Seite 1776-1784
Übergeordnetes Werk:	volume:17 ; year:2022 ; number:8 ; pages:1776-1784

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.4103/1673-5374.332156

Katalog-ID:	DOAJ074655701

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520			\|a As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.
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spelling	10.4103/1673-5374.332156 doi (DE-627)DOAJ074655701 (DE-599)DOAJ30922a910226414e9267d0360de28215 DE-627 ger DE-627 rakwb eng RC346-429 Na Wu verfasserin aut Essential role of MALAT1 in reducing traumatic brain injury 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner. angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling Neurology. Diseases of the nervous system Chong-Jie Cheng verfasserin aut Jian-Jun Zhong verfasserin aut Jun-Chi He verfasserin aut Zhao-Si Zhang verfasserin aut Zhi-Gang Wang verfasserin aut Xiao-Chuan Sun verfasserin aut Han Liu verfasserin aut In Neural Regeneration Research Wolters Kluwer Medknow Publications, 2014 17(2022), 8, Seite 1776-1784 (DE-627)545785499 (DE-600)2388460-5 18767958 nnns volume:17 year:2022 number:8 pages:1776-1784 https://doi.org/10.4103/1673-5374.332156 kostenfrei https://doaj.org/article/30922a910226414e9267d0360de28215 kostenfrei http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=8;spage=1776;epage=1784;aulast=Wu kostenfrei https://doaj.org/toc/1673-5374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2700 GBV_ILN_2817 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2022 8 1776-1784
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allfieldsSound	10.4103/1673-5374.332156 doi (DE-627)DOAJ074655701 (DE-599)DOAJ30922a910226414e9267d0360de28215 DE-627 ger DE-627 rakwb eng RC346-429 Na Wu verfasserin aut Essential role of MALAT1 in reducing traumatic brain injury 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner. angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling Neurology. Diseases of the nervous system Chong-Jie Cheng verfasserin aut Jian-Jun Zhong verfasserin aut Jun-Chi He verfasserin aut Zhao-Si Zhang verfasserin aut Zhi-Gang Wang verfasserin aut Xiao-Chuan Sun verfasserin aut Han Liu verfasserin aut In Neural Regeneration Research Wolters Kluwer Medknow Publications, 2014 17(2022), 8, Seite 1776-1784 (DE-627)545785499 (DE-600)2388460-5 18767958 nnns volume:17 year:2022 number:8 pages:1776-1784 https://doi.org/10.4103/1673-5374.332156 kostenfrei https://doaj.org/article/30922a910226414e9267d0360de28215 kostenfrei http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=8;spage=1776;epage=1784;aulast=Wu kostenfrei https://doaj.org/toc/1673-5374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2700 GBV_ILN_2817 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2022 8 1776-1784
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topic_facet	angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling Neurology. Diseases of the nervous system
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callnumber-first	R - Medicine
author	Na Wu
spellingShingle	Na Wu misc RC346-429 misc angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling misc Neurology. Diseases of the nervous system Essential role of MALAT1 in reducing traumatic brain injury
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topic_title	RC346-429 Essential role of MALAT1 in reducing traumatic brain injury angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling
topic	misc RC346-429 misc angiogenesis; controlled cortical impact; ezh2; jagged-1; lncrna; malat1; notch1; oxygen-glucose deprivation; traumatic brain injury; vascular remodeling misc Neurology. Diseases of the nervous system
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title	Essential role of MALAT1 in reducing traumatic brain injury
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title_full	Essential role of MALAT1 in reducing traumatic brain injury
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title_sort	essential role of malat1 in reducing traumatic brain injury
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title_auth	Essential role of MALAT1 in reducing traumatic brain injury
abstract	As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.
abstractGer	As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.
abstract_unstemmed	As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.
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title_short	Essential role of MALAT1 in reducing traumatic brain injury
url	https://doi.org/10.4103/1673-5374.332156 https://doaj.org/article/30922a910226414e9267d0360de28215 http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=8;spage=1776;epage=1784;aulast=Wu https://doaj.org/toc/1673-5374
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