NEAT1 regulates neuroglial cell mediating Aβ clearance via the epigenetic regulation of endocytosis-related genes expression.

Acetyl Coenzyme A / metabolism Acetylation / drug effects Alzheimer Disease / metabolism Amyloid beta-Peptides / metabolism Animals Caveolin 2 / antagonists & inhibitors Disease Models, Animal Epigenesis, Genetic Gene Expression / drug effects Histones / metabolism Mice Mice, Transgenic Neuroglia / cytology Peptide Fragments / metabolism RNA Interference RNA, Long Noncoding / antagonists & inhibitors RNA, Small Interfering / metabolism Receptor, Transforming Growth Factor-beta Type I / antagonists & inhibitors STAT3 Transcription Factor / metabolism Transforming Growth Factor beta2 / antagonists & inhibitors p300-CBP Transcription Factors / metabolism
Alzheimer’s disease Aβ Histone modification NEAT1 P300

Journal

Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402

Informations de publication

Date de publication:
Aug 2019
Historique:
received: 01 12 2018
accepted: 18 03 2019
revised: 22 02 2019
pubmed: 22 4 2019
medline: 31 7 2019
entrez: 22 4 2019
Statut: ppublish

Résumé

The accumulation of intracellular β-amyloid peptide (Aβ) is important pathological characteristic of Alzheimer's disease (AD). However, the exact underlying molecular mechanism remains to be elucidated. Here, we reported that Nuclear Paraspeckle Assembly Transcript 1 (NEAT1), a long n on-coding RNA, exhibits repressed expression in the early stage of AD and its down-regulation declines neuroglial cell mediating Aβ clearance via inhibiting expression of endocytosis-related genes. We find that NEAT1 is associated with P300/CBP complex and its inhibition affects H3K27 acetylation (H3K27Ac) and H3K27 crotonylation (H3K27Cro) located nearby to the transcription start site of many genes, including endocytosis-related genes. Interestingly, NEAT1 inhibition down-regulates H3K27Ac but up-regulates H3K27Cro through repression of acetyl-CoA generation. NEAT1 also mediates the binding between STAT3 and H3K27Ac but not H3K27Cro. Therefore, the decrease of H3K27Ac and/or the increase of H3K27Cro declines expression of multiple related genes. Collectively, this study first reveals the different roles of H3K27Ac and H3K27Cro in regulation of gene expression and provides the insight of the epigenetic regulatory mechanism of NEAT1 in gene expression and AD pathology.

Identifiants

DOI: 10.1007/s00018-019-03074-9 PMID: 31006037 PMC: PMC6647258
pubmed: 31006037
doi: 10.1007/s00018-019-03074-9
pii: 10.1007/s00018-019-03074-9
pmc: PMC6647258
doi:

Substances chimiques

Amyloid beta-Peptides 0
Cav2 protein, mouse 0
Caveolin 2 0
Histones 0
NEAT1 long non-coding RNA, mouse 0
Peptide Fragments 0
RNA, Long Noncoding 0
RNA, Small Interfering 0
STAT3 Transcription Factor 0
Tgfb2 protein, mouse 0
Transforming Growth Factor beta2 0
amyloid beta-protein (1-42) 0
Acetyl Coenzyme A 72-89-9
p300-CBP Transcription Factors EC 2.3.1.48
Receptor, Transforming Growth Factor-beta Type I EC 2.7.11.30
Tgfbr1 protein, mouse EC 2.7.11.30

Types de publication

Journal Article

Langues

eng

Pagination

3005-3018

Subventions

Organisme : National Natural Science Foundation of China
ID : 31571400
Organisme : Shenzhen Science and Technology Innovation Committee
ID : JCYJ20170405103953336
Organisme : Shenzhen Science and Technology Innovation Committee
ID : JCYJ20160226185623304
Organisme : Postdoctoral Research Foundation of China
ID : 2018M633216

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Auteurs

Ziqiang Wang (Z)

School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Yiwan Zhao (Y)

School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.

Naihan Xu (N)

Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
Open FIESTA Center, Tsinghua University, Shenzhen, 518055, China.

Shikuan Zhang (S)

School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.

Songmao Wang (S)

Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.

Yunhao Mao (Y)

Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
Open FIESTA Center, Tsinghua University, Shenzhen, 518055, China.

Yuanchang Zhu (Y)

School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.

Bing Li (B)

School of Life Sciences, Tsinghua University, Beijing, 100084, China.
Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.

Yuyang Jiang (Y)

State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.

Ying Tan (Y)

Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
Open FIESTA Center, Tsinghua University, Shenzhen, 518055, China.

Weidong Xie (W)

Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China.
Open FIESTA Center, Tsinghua University, Shenzhen, 518055, China.

Burton B Yang (BB)

School of Life Sciences, Tsinghua University, Beijing, 100084, China. byang@sri.utoronto.ca.
Department of Laboratory Medicine and Pathobiology, Sunnybrook Research Institute, University of Toronto, Toronto, Canada. byang@sri.utoronto.ca.

Yaou Zhang (Y)

School of Life Sciences, Tsinghua University, Beijing, 100084, China. zhangyo@sz.tsinghua.edu.cn.
Key Laboratory in Health Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China. zhangyo@sz.tsinghua.edu.cn.
State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, China. zhangyo@sz.tsinghua.edu.cn.
Open FIESTA Center, Tsinghua University, Shenzhen, 518055, China. zhangyo@sz.tsinghua.edu.cn.
ORCID: 0000-0002-2501-8093

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Classifications MeSH

questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Nucléotides › Ribonucléotides › Nucléotides adényliques › Coenzyme A › Acyl coenzyme A › Acétyl coenzyme A › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Métabolisme › Acylation › Acétylation › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Troubles mentaux › Troubles neurocognitifs › Démence › Maladie d'Alzheimer › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Peptides bêta-amyloïdes › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Eucaryotes › Animaux › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Phosphoprotéines › Cavéoline-2 › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Techniques d'investigation › Modèles théoriques › Modèles biologiques › Modèles animaux de maladie humaine › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Épigenèse génétique › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Phénomènes génétiques › Expression des gènes › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Nucléoprotéines › Histone › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Souris transgéniques › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Cellules › Névroglie › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Peptides › Fragments peptidiques › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Épigenèse génétique › Extinction de l'expression des gènes › Interférence par ARN › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ARN › ARN non traduit › ARN long non codant › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ARN › ARN non traduit › Petit ARN non traduit › Petit ARN interférent › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs peptidiques › Récepteur facteur croissance › Récepteurs TGF-bêta › Récepteur de type I du facteur de croissance transformant bêta › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Facteurs de transcription › Facteurs de transcription STAT › Facteur de transcription STAT-3 › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Protéines de la superfamille du TGF bêta › Facteur de croissance transformant bêta › Facteur de croissance transformant bêta-2 › NEAT1 regulates neuroglial cell mediating Aβ...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Facteurs de transcription › Facteurs de transcription CBP-p300 › NEAT1 regulates neuroglial cell mediating Aβ...