Long Non-coding RNA in Neuronal Development and Neurological Disorders

Li, Ling; Zhuang, Yingliang; Zhao, Xingsen; Li, Xuekun

doi:10.3389/fgene.2018.00744

Cited by 79 publications

(66 citation statements)

References 139 publications

(117 reference statements)

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“…Together with microRNAs and other small non-coding RNAs, expression alteration of lncRNAs could underlie pathogenesis of a broad range of human diseases [66]. Aside from their well-established roles in cancer [67], lncRNAs are crucial to cardiovascular [68], neurological [69], respiratory [70] and neurodegenerative [71] diseases. Among them, retinitis pigmentosa, an eye-related group of pathologies characterized by very heterogeneous genotypes but quite overlapping phenotypes, shows unusually complex molecular genetic causes, most of which are still unknown [72].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Analyses of lncRNAs in A2E-Stressed Retinal Epithelial Cells Unveil Advanced Links between Metabolic Impairments Related to Oxidative Stress and Retinitis Pigmentosa

et al. 2020

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Long non-coding RNAs (lncRNAs) are untranslated transcripts which regulate many biological processes. Changes in lncRNA expression pattern are well-known related to various human disorders, such as ocular diseases. Among them, retinitis pigmentosa, one of the most heterogeneous inherited disorder, is strictly related to oxidative stress. However, little is known about regulative aspects able to link oxidative stress to etiopathogenesis of retinitis. Thus, we realized a total RNA-Seq experiment, analyzing human retinal pigment epithelium cells treated by the oxidant agent N-retinylidene-N-retinylethanolamine (A2E), considering three independent experimental groups (untreated control cells, cells treated for 3 h and cells treated for 6 h). Differentially expressed lncRNAs were filtered out, explored with specific tools and databases, and finally subjected to pathway analysis. We detected 3,3'-overlapping ncRNAs, 107 antisense, 24 sense-intronic, four sense-overlapping and 227 lincRNAs very differentially expressed throughout all considered time points. Analyzed lncRNAs could be involved in several biochemical pathways related to compromised response to oxidative stress, carbohydrate and lipid metabolism impairment, melanin biosynthetic process alteration, deficiency in cellular response to amino acid starvation, unbalanced regulation of cofactor metabolic process, all leading to retinal cell death. The explored lncRNAs could play a relevant role in retinitis pigmentosa etiopathogenesis, and seem to be the ideal candidate for novel molecular markers and therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Transcriptome Analyses of lncRNAs in A2E-Stressed Retinal Epithelial Cells Unveil Advanced Links between Metabolic Impairments Related to Oxidative Stress and Retinitis Pigmentosa

et al. 2020

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“…lncRNAs are abundant in neural tissues but detected at very low levels elsewhere. lncRNAs reduce transcription, regulate the processing of mRNAs to modulate the abundance of subtly different transcripts from the same gene (alternative splicing), and influence the activity of miRNAs (108). Although evidence implicating lncRNAs in the biological embedding of experience is lacking, they are linked to mental health conditions in humans (109,110).…”

Section: Less Well-characterized Epigenetic Modificationsmentioning

confidence: 99%

Biological embedding of experience: A primer on epigenetics

Aristizabal

Anreiter

Halldorsdottir

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

171

102

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Biological embedding occurs when life experience alters biological processes to affect later life health and well-being. Although extensive correlative data exist supporting the notion that epigenetic mechanisms such as DNA methylation underlie biological embedding, causal data are lacking. We describe specific epigenetic mechanisms and their potential roles in the biological embedding of experience. We also consider the nuanced relationships between the genome, the epigenome, and gene expression. Our ability to connect biological embedding to the epigenetic landscape in its complexity is challenging and complicated by the influence of multiple factors. These include cell type, age, the timing of experience, sex, and DNA sequence. Recent advances in molecular profiling and epigenome editing, combined with the use of comparative animal and human longitudinal studies, should enable this field to transition from correlative to causal analyses.

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“…Interestingly, 15/55 differentially expressed genes in the hippocampus were lncRNAs. LncRNAs are an understudied transcriptomic component implicated in many neurological disorders (32,33), but few studies have been done regarding their role in epilepsy or SUDEP (34). Among the protein-coding genes differentially expressed in the hippocampus, GFRA1 (GDNF Family Receptor Alpha 1) was the most decreased.…”

Section: Discussionmentioning

confidence: 99%

Proteomic and Transcriptomic Analyses of the Hippocampus and Cortex in SUDEP and High-Risk SUDEP Cases

Leitner

Pires

Faustin³

et al. 2020

Preprint

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Sudden unexpected death in epilepsy (SUDEP) is the leading type of epilepsy-related death. Severely depressed brain activity in these cases may impair respiration, arousal, and protective reflexes, occurring as a prolonged postictal generalized EEG suppression (PGES) and resulting in a high-risk for SUDEP. In autopsy hippocampus and cortex, we observed no proteomic differences between SUDEP and epilepsy cases, contrasting our previously reported robust differences between epilepsy and controls. Transcriptomics in hippocampus and cortex from surgical epilepsy cases segregated by PGES identified 55 differentially expressed genes (37 protein-coding, 15 lncRNAs, three pending) in hippocampus. Overall, the SUDEP proteome and high-risk SUDEP transcriptome largely reflected other epilepsy cases in the brain regions analyzed, consistent with diverse epilepsy syndromes and comorbidities associated with SUDEP. Thus, studies with larger cohorts and different epilepsy syndromes, as well as additional anatomic regions may identify molecular mechanisms of SUDEP.

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Long Non-coding RNA in Neuronal Development and Neurological Disorders

Cited by 79 publications

References 139 publications

Transcriptome Analyses of lncRNAs in A2E-Stressed Retinal Epithelial Cells Unveil Advanced Links between Metabolic Impairments Related to Oxidative Stress and Retinitis Pigmentosa

Transcriptome Analyses of lncRNAs in A2E-Stressed Retinal Epithelial Cells Unveil Advanced Links between Metabolic Impairments Related to Oxidative Stress and Retinitis Pigmentosa

Biological embedding of experience: A primer on epigenetics

Proteomic and Transcriptomic Analyses of the Hippocampus and Cortex in SUDEP and High-Risk SUDEP Cases

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