ArticleMedical science monitor : international medical journal of experimental and clinical research2018
A Possible Role for Long Interspersed Nuclear Elements-1 (LINE-1) in Huntington's Disease Progression.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Epigenetic pharmacology in aging: from mechanisms to therapies for age-related disorders.Frontiers in pharmacology · 2025Review
- Comprehensive profiling of L1 retrotransposons in mouse.Nucleic acids research · 2024Article
- Repetitive elements in aging and neurodegeneration.Trends in genetics : TIG · 2023Review
- The Role of Transposable Elements of the Human Genome in Neuronal Function and Pathology.International journal of molecular sciences · 2022Review
- DNA Methylation in Huntington's Disease.International journal of molecular sciences · 2021Review
- Analysis of LINE1 Retrotransposons in Huntington's Disease.Frontiers in cellular neuroscience · 2021Article
- Article
- Exploratory analysis of transposable elements expression in the C. elegans early embryo.BMC bioinformatics · 2019Article
- Brain organoids and insights on human evolution.F1000Research · 2019Review
- Properties of LINE-1 proteins and repeat element expression in the context of amyotrophic lateral sclerosis.Mobile DNA · 2018Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Recent studies have shown that increased mobilization of Long Interspersed Nuclear Elements-1 (L1) can promote the pathophysiology of multiple neurological diseases. However, its role in Huntington's disease (HD) remains unknown. MATERIAL AND METHODS R6/2 mice - a common mouse model of HD - were used to evaluate changes in L1 mobilization. Pyrosequencing was used to evaluate methylation content changes. L1-ORF1 and L1-ORF2 expression analysis were evaluated by RT-PCR and immunoblotting. Changes in pro-survival signaling were evaluated by L1-ORF overexpression studies and validated in the mouse model by immunohistochemistry and immunoblotting. RESULTS We found an increased mobilization of L1 elements in the caudate genome of R6/2 mice (p<0.05) - a common mouse model of HD - but not in wild-type mice. Subsequent pyrosequencing and expression analysis showed that the L1 elements were hypomethylated and their respective ORFs were overexpressed in the affected tissues. In addition, a significant decrease in the pro-survival proteins such as the phosphoproteins of AKT target proteins, mTORC1 activity, and AMPK alpha levels was observed with the increase in the expression L1-ORF2. CONCLUSIONS These findings indicate that hyperactive retrotransposition of L1 triggers a downstream signaling pathway affecting the neuronal survival pathways via downregulation of mTORC1 activity and AMPKalpha and increasing apoptosis in neurons.
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