Bioinformatic analysis of microRNA expression in Huntington's disease

Dong, Xiaoyu; Cong, Shuyan

doi:10.3892/mmr.2018.9238

Cited by 12 publications

(15 citation statements)

References 54 publications

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“…A former bioinformatic analysis of miRNA expression identified 33 possible miRNA-target relationships in post-mortem brain samples of HD patients compared to control individuals [38]. We found no overlap between these predictions and the miRNA-target pairs retained by miRAMINT, which is expected as the study of post-mortem brain samples relied on a simple overlap analysis (based on binding sites in TargetScan) between lists of differentially expressed miRNAs and mRNAs [39] and as miRNA regulation in the humain brain could significantly differ from that in the mouse brain.…”

Section: Discussionmentioning

confidence: 99%

Combining feature selection and shape analysis uncovers precise rules for miRNA regulation in Huntington’s disease mice

et al. 2020

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Background: MicroRNA (miRNA) regulation is associated with several diseases, including neurodegenerative diseases. Several approaches can be used for modeling miRNA regulation. However, their precision may be limited for analyzing multidimensional data. Here, we addressed this question by integrating shape analysis and feature selection into miRAMINT, a methodology that we used for analyzing multidimensional RNA-seq and proteomic data from a knock-in mouse model (Hdh mice) of Huntington's disease (HD), a disease caused by CAG repeat expansion in huntingtin (htt). This dataset covers 6 CAG repeat alleles and 3 age points in the striatum and cortex of Hdh mice. Results: Remarkably, compared to previous analyzes of this multidimensional dataset, the miRAMINT approach retained only 31 explanatory striatal miRNA-mRNA pairs that are precisely associated with the shape of CAG repeat dependence over time, among which 5 pairs with a strong change of target expression levels. Several of these pairs were previously associated with neuronal homeostasis or HD pathogenesis, or both. Such miRNA-mRNA pairs were not detected in cortex. Conclusions: These data suggest that miRNA regulation has a limited global role in HD while providing accuratelyselected miRNA-target pairs to study how the brain may compute molecular responses to HD over time. These data also provide a methodological framework for researchers to explore how shape analysis can enhance multidimensional data analytics in biology and disease.

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Section: Discussionmentioning

confidence: 99%

Combining feature selection and shape analysis uncovers precise rules for miRNA regulation in Huntington’s disease mice

et al. 2020

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“…A former bioinformatic analysis of miRNA expression identified 33 possible miRNA-target relationships in post-mortem brain samples of HD patients compared to control individuals [37].…”

Section: Discussionmentioning

confidence: 99%

Combining feature selection and shape analysis uncovers precise rules for miRNA regulation in Huntington’s disease mice

Mégret

Nair

Dancourt

et al. 2020

Preprint

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BackgroundMicroRNA (miRNA) regulation is associated with several diseases, including neurodegenerative diseases. Several approaches can be used for modeling miRNA regulation. However, their precision may be limited for analyzing multidimensional data. Here, we addressed this question by integrating shape analysis and feature selection into miRAMINT, a methodology that we used for analyzing multidimensional RNA-seq and proteomic data from a knock-in mouse model (Hdh mice) of Huntington's disease (HD), a disease caused by CAG repeat expansion in huntingtin (htt).This dataset covers 6 CAG repeat alleles and 3 age points in the striatum and cortex of Hdh mice. ResultsRemarkably, compared to previous analyzes of this multidimensional dataset, the miRAMINT approach retained only 31 explanatory striatal miRNA-mRNA pairs that are precisely associated with the shape of CAG repeat dependence over time, among which 5 pairs with a strong change of target expression levels. Several of these pairs were previously associated with neuronal homeostasis or HD pathogenesis, or both. Such miRNA-mRNA pairs were not detected in cortex. ConclusionsThese data suggest that miRNA regulation has a limited global role in HD while providing accurately-selected miRNA-target pairs to study how the brain may compute molecular responses to HD over time. These data also provide a methodological framework for researchers to explore how shape analysis can enhance multidimensional data analytics in biology and disease.2

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“…A smaller number of studies have explored the miRNA profiles in HD. These profiles are found in the brain [ 159 , 160 , 161 ], plasma [ 162 ], and CSF [ 163 ] of HD patients and in the brain of HD mouse models [ 164 , 165 , 166 , 167 ]. No common miRNAs are found between the profiles performed in HD patients, but there are two miRNAs, miR-10b-5p and miR-10a-5p, that are upregulated in the brain of both HD patients and mouse models.…”

Section: Epigenetic Changes In Prion-like Diseasesmentioning

confidence: 99%

Epigenetic Changes in Prion and Prion-like Neurodegenerative Diseases: Recent Advances, Potential as Biomarkers, and Future Perspectives

Hernaiz

Toivonen²,

Bolea³

et al. 2022

IJMS

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Prion diseases are transmissible spongiform encephalopathies (TSEs) caused by a conformational conversion of the native cellular prion protein (PrPC) to an abnormal, infectious isoform called PrPSc. Amyotrophic lateral sclerosis, Alzheimer’s, Parkinson’s, and Huntington’s diseases are also known as prion-like diseases because they share common features with prion diseases, including protein misfolding and aggregation, as well as the spread of these misfolded proteins into different brain regions. Increasing evidence proposes the involvement of epigenetic mechanisms, namely DNA methylation, post-translational modifications of histones, and microRNA-mediated post-transcriptional gene regulation in the pathogenesis of prion-like diseases. Little is known about the role of epigenetic modifications in prion diseases, but recent findings also point to a potential regulatory role of epigenetic mechanisms in the pathology of these diseases. This review highlights recent findings on epigenetic modifications in TSEs and prion-like diseases and discusses the potential role of such mechanisms in disease pathology and their use as potential biomarkers.

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Bioinformatic analysis of microRNA expression in Huntington's disease

Cited by 12 publications

References 54 publications

Combining feature selection and shape analysis uncovers precise rules for miRNA regulation in Huntington’s disease mice

Combining feature selection and shape analysis uncovers precise rules for miRNA regulation in Huntington’s disease mice

Combining feature selection and shape analysis uncovers precise rules for miRNA regulation in Huntington’s disease mice

Epigenetic Changes in Prion and Prion-like Neurodegenerative Diseases: Recent Advances, Potential as Biomarkers, and Future Perspectives

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