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Long non-coding RNA NEAT1_1 ameliorates TDP-43 toxicity in in vivo models of TDP-43 proteinopathy

RNA biology, 2021-11, Vol.18 (11), p.1546-1554 [Peer Reviewed Journal]

2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2020 ;2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2020 The Author(s) ;ISSN: 1547-6286 ;EISSN: 1555-8584 ;DOI: 10.1080/15476286.2020.1860580 ;PMID: 33427561

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Title:
Long non-coding RNA NEAT1_1 ameliorates TDP-43 toxicity in in vivo models of TDP-43 proteinopathy
Author: Matsukawa, Koji ; Kukharsky, Michail S. ; Park, Sei-Kyoung ; Park, Sangeun ; Watanabe, Naruaki ; Iwatsubo, Takeshi ; Hashimoto, Tadafumi ; Liebman, Susan W. ; Shelkovnikova, Tatyana A.
Subjects: ALS ; Alzheimer's disease ; Amyotrophic Lateral Sclerosis - etiology ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - pathology ; Amyotrophic Lateral Sclerosis - prevention & control ; Animals ; Brain - metabolism ; Brain - pathology ; Brief Communication ; Disease Models, Animal ; DNA-Binding Proteins - toxicity ; drosophila ; Drosophila melanogaster ; frontotemporal dementia ; Frontotemporal Dementia - etiology ; Frontotemporal Dementia - metabolism ; Frontotemporal Dementia - pathology ; Frontotemporal Dementia - prevention & control ; FTLD ; FUS ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; NEAT1 ; Neuroblastoma - etiology ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; Neuroblastoma - prevention & control ; neurodegeneration ; proteinopathy ; Rapid Communication ; RNA, Long Noncoding - administration & dosage ; RNA, Long Noncoding - genetics ; Saccharomyces cerevisiae ; TDP-43 ; TDP-43 Proteinopathies - etiology ; TDP-43 Proteinopathies - metabolism ; TDP-43 Proteinopathies - pathology ; TDP-43 Proteinopathies - prevention & control ; yeast
Is Part Of: RNA biology, 2021-11, Vol.18 (11), p.1546-1554
Description: Pathological changes involving TDP-43 protein ('TDP-43 proteinopathy') are typical for several neurodegenerative diseases, including frontotemporal lobar degeneration (FTLD). FTLD-TDP cases are characterized by increased binding of TDP-43 to an abundant lncRNA, NEAT1, in the cortex. However it is unclear whether enhanced TDP-43-NEAT1 interaction represents a protective mechanism. We show that accumulation of human TDP-43 leads to upregulation of the constitutive NEAT1 isoform, NEAT1_1, in cultured cells and in the brains of transgenic mice. Further, we demonstrate that overexpression of NEAT1_1 ameliorates TDP-43 toxicity in Drosophila and yeast models of TDP-43 proteinopathy. Thus, NEAT1_1 upregulation may be protective in TDP-43 proteinopathies affecting the brain. Approaches to boost NEAT1_1 expression in the CNS may prove useful in the treatment of these conditions.
Publisher: United States: Taylor & Francis
Language: English
Identifier: ISSN: 1547-6286
EISSN: 1555-8584
DOI: 10.1080/15476286.2020.1860580
PMID: 33427561
Source: Taylor & Francis Open Access
GFMER Free Medical Journals
MEDLINE
PubMed Central

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Long non-coding RNA NEAT1_1 ameliorates TDP-43 toxicity in in vivo models of TDP-43 proteinopathy

2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2020 ;2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2020 The Author(s) ;ISSN: 1547-6286 ;EISSN: 1555-8584 ;DOI: 10.1080/15476286.2020.1860580 ;PMID: 33427561

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