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Miska, Eric A.; Alvarez-Saavedra, Ezequiel; Townsend, Matthew; Yoshii, Akira; Šestan, Nenad; Rakić, Paško; Constantine‐Paton, Martha; Horvitz, H. Robert

doi:10.1186/gb-2004-5-9-r68

Cited by 717 publications

(255 citation statements)

References 55 publications

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“…Previous studies also suggested that miRNA alterations occur during neural stem cell differentiation and morphological development of the mammalian brain 29, 32. One member of our group also proved that a significant difference in miRNA expression pattern is a possible marker of anencephaly 17.…”

Section: Discussionsupporting

confidence: 70%

“…Interestingly, at least half of the promoter regions for miRNAs are predicted to be in close proximity to CpG islands and their methylation frequency is predicted to be at least one order of magnitude higher than that of protein‐coding genes 12. New studies in human cell lines have also shown that folic acid deficiency and DNA hypomethylation can lead to the misexpression of miRNAs 26, 27, 28, 29. Against this background, a more thorough understanding of how folate deficiency contributes to the misexpression of miRNAs and their roles in NTDs should help us to clarify the mechanism behind miRNA regulation in NTDs.…”

Section: Introductionmentioning

confidence: 99%

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Folate deficiency disturbs hsa‐let‐7 g level through methylation regulation in neural tube defects

Wang

Shangguan

et al. 2017

J Cellular Molecular Medi

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Folic acid deficiency during pregnancy is believed to be a high‐risk factor for neural tube defects (NTDs). Disturbed epigenetic modifications, including miRNA regulation, have been linked to the pathogenesis of NTDs in those with folate deficiency. However, the mechanism by which folic acid‐regulated miRNA influences this pathogenesis remains unclear. It is believed that DNA methylation is associated with dysregulated miRNA expression. To clarify this issue, here we measured the methylation changes of 22 miRNAs in 57 human NTD cases to explore whether such changes are involved in miRNA regulation in NTD cases through folate metabolism. In total, eight of the 22 miRNAs tested reduced their methylation modifications in NTD cases, which provide direct evidence of the roles of interactions between DNA methylation and miRNA level in these defects. Among the findings, there was a significant association between folic acid concentration and hsa‐let‐7 g methylation level in NTD cases. Hypomethylation of hsa‐let‐7 g increased its own expression level in both NTD cases and cell models, which indicated that hsa‐let‐7 g methylation directly regulates its own expression. Overexpression of hsa‐let‐7 g, along with its target genes, disturbed the migration and proliferation of SK‐N‐SH cells, implying that hsa‐let‐7 g plays important roles in the prevention of NTDs by folic acid. In summary, our data suggest a relationship between aberrant methylation of hsa‐let‐7 g and disturbed folate metabolism in NTDs, implying that improvements in nutrition during early pregnancy may prevent such defects, possibly via the donation of methyl groups for miRNAs.

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Section: Discussionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Folate deficiency disturbs hsa‐let‐7 g level through methylation regulation in neural tube defects

Wang

Shangguan

et al. 2017

J Cellular Molecular Medi

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“…In the construction of brain cell-specific miRNA array panels, 13 individual brain-enriched miRNAs and human 5S ribosomal RNA (5S rRNA) were spotted onto GeneScreen Plus nylon membranes using a Biomek® 2000 laboratory automation workstation (Beckmann, Fullerton, CA) and were crosslinked, baked, hybridized and probed according to the manufacturer's protocol (NEN® Research Products, Boston MA) [7,[10][11][12]. A guanidine isothiocyanate-and silica gel-based membrane total RNA purification system and miRNA isolation kit (PureLink™ Invitrogen, Carlsbad, CA) were used to isolate total small RNAs (5S rRNA, tRNA and miRNA) from magnesium-, aluminum-and iron-plus aluminum-sulfate treated HN cells.…”

Section: Footnote 1 -Experimental Detailsmentioning

confidence: 99%

“…Through their complementary base-pairing with the 3′ UTRs of target mRNA, miRNAs function in transcriptional processing or provide guidance for further mRNA modification [7][8][9][10][11][12][13][14][15][16][17]. The variable expression of miRNAs during cell growth and aging has suggested a role for miRNA in the regulation of gene expression during development and differentiation, and while human genomes encode several hundred different miRNAs, a significantly smaller sub-set is either enriched in the brain or specific to that organ [7,[10][11][12]. Although up-regulated miRNAs are generally regarded as negative regulators of these multiple processes, down-regulation of miRNA might be expected to enhance mRNA translation and thereby up-regulate the expression of specific genes.…”

mentioning

confidence: 99%

Induction of specific micro RNA (miRNA) species by ROS-generating metal sulfates in primary human brain cells

Lukiw

Pogue

2007

Journal of Inorganic Biochemistry

193

222

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Iron-and aluminum-sulfate together, at nanomolar concentrations, trigger the production of reactive oxygen species (ROS) in cultures of human brain cells. Previous studies have shown that following ROS induction, a family of pathogenic brain genes that promote inflammatory signalling, cellular apoptosis and brain cell death is significantly over-expressed. Notably, iron-and aluminum-sulfate induce genes in cultured human brain cells that exhibit expression patterns similar to those observed to be up-regulated in moderate-to late-stage Alzheimer's disease (AD). In this study we have extended our investigations to analyze the expression of micro RNA (miRNA) populations in ironand aluminum-sulfate treated human neural cells in primary culture. The main finding was that these ROS-generating neurotoxic metal sulfates also up-regulate a specific set of miRNAs that includes miR-9, miR-125b and miR-128. Notably, these same miRNAs are up-regulated in AD brain. These findings further support the idea that iron-and aluminum-sulfates induce genotoxicity via a ROS-* Corresponding Author: Walter J. Lukiw, MS, PhD, e-mail: wlukiw@lsuhsc.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. FOOTNOTE 1 -Experimental detailsIn the construction of brain cell-specific miRNA array panels, 13 individual brain-enriched miRNAs and human 5S ribosomal RNA (5S rRNA) were spotted onto GeneScreen Plus nylon membranes using a Biomek® 2000 laboratory automation workstation (Beckmann, Fullerton, CA) and were crosslinked, baked, hybridized and probed according to the manufacturer's protocol (NEN® Research Products, Boston MA) [7,[10][11][12]. A guanidine isothiocyanate-and silica gel-based membrane total RNA purification system and miRNA isolation kit (PureLink™ Invitrogen, Carlsbad, CA) were used to isolate total small RNAs (5S rRNA, tRNA and miRNA) from magnesium-, aluminum-and iron-plus aluminum-sulfate treated HN cells. Total RNA concentrations and spectral purity were quantified using RNA 6000 Nano LabChip analysis and a 2100 Spectral Analyzer (Caliper Technologies, Mountainview, CA; Agilent Technologies, Palo Alto, CA) [1,4,5,7]. 28S/18S ratios consistently exceeded 1.4 and the A 260/280 of total RNA (based on peak area) was typically ≥1.8. Poly A+ messenger RNA was found to range in size from 0.5−8 kilobases. In a preliminary screen, miRNA arrays were probed with total labeled miRNAs isolated from 3 week old HN cells that had been exposed to 100 nM magnesium-sulfate (control), or aluminum-sulfate, or aluminum-plus iron-sulfate, for 7 days, or about one-third of their in vitro life-span [1]. ...

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“…The set of microRNAs changed expression upon induction of cultured cells to neurogenic status. MicroRNAs are temporally regulated during brain devel opment (shown in rodents) [9].…”

mentioning

confidence: 99%

Small RNAs in Human Brain Development and Disorders

Rogaev

2005

Biochemistry (Moscow)

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Abstract-Small RNA is a variable and abundant type of non coding RNAs in brain. The function of these RNAs is main ly unknown. A specific class of small RNA, microRNA, is dynamically regulated in neurogenesis and in embryo brain devel opment. The genes for synaptic formation and some mental retardation disorders are putative targets for microRNA pre dicted by computational algorithms. The molecular pathways for mental development, common forms of autisms, schizo phrenia, and affective disorders have yet to be elucidated. The hypothesis proposed here is that small regulatory RNAs, specifically microRNAs, play a role in human brain development and pathogenesis of brain disorders, especially of neu rodevelopmental conditions. Pilot tests using comprehensive arrays of microRNAs demonstrate that microRNAs derived from postmortem human brains are applicable for microRNA expression profiling. The abundant expression of many reg ulatory small RNAs in human brain implies their biological role that must be tested by functional assays in neurons and by genetic and comparative expression profiling.

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Abstract: A microarray technology suitable for analyzing the expression of microRNAs and of other small RNAs was used to determine the microRNA expression profile during mouse-brain development and observed a temporal wave of gene expression of sequential classes of microRNAs.

Cited by 717 publications

References 55 publications

Folate deficiency disturbs hsa‐let‐7 g level through methylation regulation in neural tube defects

Folate deficiency disturbs hsa‐let‐7 g level through methylation regulation in neural tube defects

Induction of specific micro RNA (miRNA) species by ROS-generating metal sulfates in primary human brain cells

Small RNAs in Human Brain Development and Disorders

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