MicroRNA-29 is an essential regulator of brain maturation through regulation of CH methylation

Swahari, Vijay; Nakamura, Ayumi; Hollville, Émilie; Stroud, Hume; Simon, Jeremy M.; Ptacek, Travis; Beck, Matthew V.; Flowers, Cornelius; Guo, Jiqing; Plestant, Charlotte; Liang, Jie; Kurtz, C. Lisa; Kanke, Matt; Hammond, Scott M.; He, You Wen; Anton, E. S.; Sethupathy, Praveen; Moy, Sheryl S.; Greenberg, Michael E.; Deshmukh, Mohanish

doi:10.1016/j.celrep.2021.108946

Cited by 36 publications

(46 citation statements)

References 91 publications

(108 reference statements)

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“…Most studies examining human cortex have found that the level of at least one member of the miR-29 family increases significantly during postnatal development [44,45,47] (but also see [48]). Studies in macaque, pig, rat, and mouse have demonstrated that postnatal miR-29 upregulation with age is highly conserved among mammals [45,49,51,[53][54][55][80][81][82][83]. Notably, Swahari et al [55] examined the levels of miR-29 in mouse cortex at P0-P60 and observed a robust increase in all three family members before the onset of adolescence (P0-P20) and during the transition from early to mid-adolescence (P20-P40).…”

Section: The Mir-29 Family and Mir-132-3p Levels Increase With Age And May Be Dysregulated In Sczmentioning

confidence: 99%

“…Studies in macaque, pig, rat, and mouse have demonstrated that postnatal miR-29 upregulation with age is highly conserved among mammals [45,49,51,[53][54][55][80][81][82][83]. Notably, Swahari et al [55] examined the levels of miR-29 in mouse cortex at P0-P60 and observed a robust increase in all three family members before the onset of adolescence (P0-P20) and during the transition from early to mid-adolescence (P20-P40). Napoli et al [83] also observed a robust increase of miR-29a-3p in mouse visual cortex prior to adolescence (P10-P25) and throughout adolescence (P25-P60) [83].…”

Section: The Mir-29 Family and Mir-132-3p Levels Increase With Age And May Be Dysregulated In Sczmentioning

confidence: 99%

“…Both miR-29 and miR-132-3p target the DNA methyltransferase DNMT3A and may contribute to its downregulation during adolescence [10,55]. DNMT3A specifically catalyzes CH-methylation [248], where H indicates T, A, or C nucleotides.…”

Section: Shared Roles Of Mir-29 and Mir-132-3p: Cortical Ocular Dominance Plasticity And Dnmt3amentioning

confidence: 99%

“…The loss of DNMT3A disrupts early brain development; however, failure to downregulate DNMT3A during adolescence is devastating to adult brain function. The mutation of miR-29-binding sites in Dnmt3a in mice leads to elevated DNMT3A protein levels, behavioral abnormalities (e.g., limb clasping), increased seizure susceptibility, and reduced lifespan [55]. Dnmt3a mRNA is also upregulated in response to monocular deprivation, and treatment with the DNA methyltransferase inhibitor RG108 blocks ocular dominance plasticity [251], suggesting that Dnmt3a downregulation by miR-29 and miR-132-3p contributes to these miRNAs' roles in ocular dominance plasticity.…”

Section: Shared Roles Of Mir-29 and Mir-132-3p: Cortical Ocular Dominance Plasticity And Dnmt3amentioning

confidence: 99%

“…During adolescence, the miRNAs are incorrectly expressed, leading to dysregulation of their targets and disruption of neurodevelopment. For example, both miR-29 and miR-132-3p downregulate DNMT3A during adolescence and adulthood [10,55], but neither miRNA is essential for regulating DNMT3A levels during early postnatal development, when they are virtually undetectable. Genetic or environmental factors that inhibit miR-29 and miR-132-3p most likely have no effect on DNMT3A levels during early development because these miRNAs are not essential during that time.…”

Section: Direct Mechanism: Aberrations In Mirnas During Adolescence Disrupt Adolescent Brain Maturation and Cause Disease Onsetmentioning

confidence: 99%

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MicroRNAs in the Onset of Schizophrenia

Thomas

Zakharenko

2021

Cells

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Mounting evidence implicates microRNAs (miRNAs) in the pathology of schizophrenia. These small noncoding RNAs bind to mRNAs containing complementary sequences and promote their degradation and/or inhibit protein synthesis. A single miRNA may have hundreds of targets, and miRNA targets are overrepresented among schizophrenia-risk genes. Although schizophrenia is a neurodevelopmental disorder, symptoms usually do not appear until adolescence, and most patients do not receive a schizophrenia diagnosis until late adolescence or early adulthood. However, few studies have examined miRNAs during this critical period. First, we examine evidence that the miRNA pathway is dynamic throughout adolescence and adulthood and that miRNAs regulate processes critical to late neurodevelopment that are aberrant in patients with schizophrenia. Next, we examine evidence implicating miRNAs in the conversion to psychosis, including a schizophrenia-associated single nucleotide polymorphism in MIR137HG that is among the strongest known predictors of age of onset in patients with schizophrenia. Finally, we examine how hemizygosity for DGCR8, which encodes an obligate component of the complex that synthesizes miRNA precursors, may contribute to the onset of psychosis in patients with 22q11.2 microdeletions and how animal models of this disorder can help us understand the many roles of miRNAs in the onset of schizophrenia.

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Section: The Mir-29 Family and Mir-132-3p Levels Increase With Age And May Be Dysregulated In Sczmentioning

confidence: 99%

Section: The Mir-29 Family and Mir-132-3p Levels Increase With Age And May Be Dysregulated In Sczmentioning

confidence: 99%

Section: Shared Roles Of Mir-29 and Mir-132-3p: Cortical Ocular Dominance Plasticity And Dnmt3amentioning

confidence: 99%

Section: Shared Roles Of Mir-29 and Mir-132-3p: Cortical Ocular Dominance Plasticity And Dnmt3amentioning

confidence: 99%

Section: Direct Mechanism: Aberrations In Mirnas During Adolescence Disrupt Adolescent Brain Maturation and Cause Disease Onsetmentioning

confidence: 99%

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MicroRNAs in the Onset of Schizophrenia

Thomas

Zakharenko

2021

Cells

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Micromanaging the neuroendocrine system – A review on miR‐7 and the other physiologically relevant miRNAs in the hypothalamic–pituitary axis

Zacharjasz,

Sztachera,

Smuszkiewicz

et al. 2024

FEBS Letters

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The hypothalamic–pituitary axis is central to the functioning of the neuroendocrine system and essential for regulating physiological and behavioral homeostasis and coordinating fundamental body functions. The expanding line of evidence shows the indispensable role of the microRNA pathway in regulating the gene expression profile in the developing and adult hypothalamus and pituitary gland. Experiments provoking a depletion of miRNA maturation in the context of the hypothalamic–pituitary axis brought into focus a prominent involvement of miRNAs in neuroendocrine functions. There are also a few individual miRNAs and miRNA families that have been studied in depth revealing their crucial role in mediating the regulation of fundamental processes such as temporal precision of puberty timing, hormone production, fertility and reproduction capacity, and energy balance. Among these miRNAs, miR‐7 was shown to be hypothalamus‐enriched and the top one highly expressed in the pituitary gland, where it has a profound impact on gene expression regulation. Here, we review miRNA profiles, knockout phenotypes, and miRNA interaction (targets) in the hypothalamic–pituitary axis that advance our understanding of the roles of miRNAs in mammalian neurosecretion and related physiology.

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Genetically engineered neural stem cells (NSCs) therapy for neurological diseases; state‐of‐the‐art

Lutfi Ismaeel,

Makki AlHassani,

S. Alazragi

et al. 2023

Biotechnology Progress

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Neural stem cells (NSCs) are multipotent stem cells with remarkable self‐renewal potential and also unique competencies to differentiate into neurons, astrocytes, and oligodendrocytes (ODCs) and improve the cellular microenvironment. In addition, NSCs secret diversity of mediators, including neurotrophic factors (e.g., BDNF, NGF, GDNF, CNTF, and NT‐3), pro‐angiogenic mediators (e.g., FGF‐2 and VEGF), and anti‐inflammatory biomolecules. Thereby, NSCs transplantation has become a reasonable and effective treatment for various neurodegenerative disorders by their capacity to induce neurogenesis and vasculogenesis and dampen neuroinflammation and oxidative stress. Nonetheless, various drawbacks such as lower migration and survival and less differential capacity to a particular cell lineage concerning the disease pathogenesis hinder their application. Thus, genetic engineering of NSCs before transplantation is recently regarded as an innovative strategy to bypass these hurdles. Indeed, genetically modified NSCs could bring about more favored therapeutic influences post‐transplantation in vivo, making them an excellent option for neurological disease therapy. This review for the first time offers a comprehensive review of the therapeutic capability of genetically modified NSCs rather than naïve NSCs in neurological disease beyond brain tumors and sheds light on the recent progress and prospect in this context.

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MicroRNA-29 is an essential regulator of brain maturation through regulation of CH methylation

Cited by 36 publications

References 91 publications

MicroRNAs in the Onset of Schizophrenia

MicroRNAs in the Onset of Schizophrenia

Micromanaging the neuroendocrine system – A review on miR‐7 and the other physiologically relevant miRNAs in the hypothalamic–pituitary axis

Genetically engineered neural stem cells (NSCs) therapy for neurological diseases; state‐of‐the‐art

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