Distinct expression of NEAT1 isoforms in Parkinson’s disease models suggests different roles of the variants during the disease course.

Publication date: Apr 15, 2025

Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. Recently long non-coding RNAs (lncRNAs) have emerged as possible molecular hubs in the diverse pathomechanisms of the disease. Among them, NEAT1 gained particular interest due to findings suggesting both protective and deleterious effects of this lncRNA in PD models. The aim of this study was to clarify some of the contradictions among data that appeared in recent publications concerning NEAT1 effects. For this, we determined whether pharmacological increase of NEAT1 levels worsened the detrimental effect of MPP + in the SH-SY5Y cell model, and whether the levels of the short and long isoform of the lncRNA changed differently upon short and extended MPTP treatment in an MPTP-induced mouse model of PD. Our findings suggest differential expression of NEAT1/Neat1 isoforms in MPP + /MPTP-induced PD models, which is in accord with the proposed role of the lncRNA in the general stress response. We propose that first an early up-regulation of Neat1_2 is dominant. The level of Neat1_2 then decreases as pathology progresses, resulting in a shift in the ratio of the two isoforms towards a higher level of Neat1_1 accompanied by damage of the central nervous system.

Open Access PDF

Concepts Keywords
Nervous Animals
Parkinson Cell Line, Tumor
Pathology Disease Models, Animal
Pharmacological Gene Expression Regulation
Worldwide Humans
lncRNA
Male
MAO
Mice
MPTP
NEAT1
Neat1
Neurodegeneration
Parkinson Disease
Parkinson’s disease
Protein Isoforms
Protein Isoforms
RNA Isoforms
RNA Isoforms
RNA, Long Noncoding
RNA, Long Noncoding

Semantics

Type Source Name
disease MESH Parkinson’s disease
disease MESH neurodegenerative disease
disease MESH ALS Amyotrophic lateral sclerosis
drug DRUGBANK Sulforaphane
disease MESH shock
drug DRUGBANK Dopamine
drug DRUGBANK Serotonin
drug DRUGBANK Coenzyme M
drug DRUGBANK Oxygen
drug DRUGBANK Norepinephrine
disease MESH hypoxia
pathway REACTOME Translation
disease MESH neuroblastoma
pathway KEGG Amyotrophic lateral sclerosis
pathway REACTOME Apoptosis
drug DRUGBANK Aspartame
pathway REACTOME Neurodegenerative Diseases
disease MESH spinocerebellar ataxia
pathway KEGG Spinocerebellar ataxia
pathway REACTOME Autophagy
disease MESH oxidative damage
pathway REACTOME Metabolism
disease MESH neurological disorders
drug DRUGBANK Streptomycin
drug DRUGBANK Phosphate ion
drug DRUGBANK Ethanol
drug DRUGBANK Water
drug DRUGBANK Isoflurane
drug DRUGBANK Levodopa
drug DRUGBANK Isoprenaline
drug DRUGBANK Indole
drug DRUGBANK Pidolic Acid
drug DRUGBANK Theophylline
drug DRUGBANK Perchlorate
drug DRUGBANK Dipotassium phosphate
drug DRUGBANK Monopotassium phosphate
drug DRUGBANK Edetic Acid
drug DRUGBANK Flunarizine
disease MESH cancer
drug DRUGBANK Thiocolchicoside
disease MESH parkinsonism
pathway REACTOME Mitochondrial biogenesis
pathway KEGG Parkinson disease
disease MESH inflammation
pathway KEGG Ferroptosis
disease MESH prostate cancer
pathway KEGG Prostate cancer
drug DRUGBANK Guanosine
drug DRUGBANK Carboxyamidotriazole
drug DRUGBANK NADH
drug DRUGBANK Phenol
pathway REACTOME Reproduction
disease MESH Disease Models Animal

Original Article

(Visited 1 times, 1 visits today)

Leave a Comment

Your email address will not be published. Required fields are marked *