Maternal alcohol consumption and altered miRNAs in the developing fetus: Context and future perspectives

Mandal, Chanchal; Halder, Debasish; Jung, Kyoung Hwa; Chai, Young Gyu

doi:10.1002/jat.3504

Cited by 23 publications

(10 citation statements)

References 48 publications

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“…Importantly, smoking and alcohol consumption, which are associated not only with cancer but also with other diseases, alter miRNA expression in the serum and cells [37–41]. During development, maternal alcohol consumption directly influences miRNA expression in mice and zebrafish [42–44]. Recent studies suggest that miRNAs may pass through the placenta from mothers to embryos to directly regulate embryogenesis [45, 46].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-374a, -4680, and -133b suppress cell proliferation through the regulation of genes associated with human cleft palate in cultured human palate cells

Suzuki

Gajera

et al. 2019

BMC Med Genomics

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Background Cleft palate (CP) is the second most common congenital birth defect; however, the relationship between CP-associated genes and epigenetic regulation remains largely unknown. In this study, we investigated the contribution of microRNAs (miRNAs) to cell proliferation and regulation of genes involved in CP development. Methods In order to identify all genes for which mutations or association/linkage have been found in individuals with CP, we conducted a systematic literature search, followed by bioinformatics analyses for these genes. We validated the bioinformatics results experimentally by conducting cell proliferation assays and miRNA-gene regulatory analyses in cultured human palatal mesenchymal cells treated with each miRNA mimic. Results We identified 131 CP-associated genes in the systematic review. The bioinformatics analysis indicated that the CP genes were associated with signaling pathways, microRNAs (miRNAs), metabolic pathways, and cell proliferation. A total 17 miRNAs were recognized as potential modifiers of human CP genes. To validate miRNA function in cell proliferation, a main cause of CP, we conducted cell proliferation/viability assays for the top 11 candidate miRNAs from our bioinformatics analysis. Overexpression of miR-133b, miR-374a-5p, and miR-4680-3p resulted in a more than 30% reduction in cell proliferation activity in human palatal mesenchymal cell cultures. We found that several downstream target CP genes predicted by the bioinformatics analyses were significantly downregulated through induction of these miRNAs ( FGFR1 , GCH1 , PAX7 , SMC2 , and SUMO1 by miR-133b; ARNT , BMP2 , CRISPLD1 , FGFR2 , JARID2 , MSX1 , NOG , RHPN2 , RUNX2 , WNT5A and ZNF236 by miR - 374a-5p; and ERBB2 , JADE1 , MTHFD1 and WNT5A by miR-4680-3p) in cultured cells. Conclusions Our results indicate that miR-374a-5p, miR-4680-3p, and miR-133b regulate expression of genes that are involved in the etiology of human CP, providing insight into the association between CP-associated genes and potential targets of miRNAs in palate development. Electronic supplementary material The online version of this article (10.1186/s12920-019-0546-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-374a, -4680, and -133b suppress cell proliferation through the regulation of genes associated with human cleft palate in cultured human palate cells

Suzuki

Gajera

et al. 2019

BMC Med Genomics

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“…Extensive alcohol-mediated changes in miRNA and miRNA-target gene expression have been observed in utero that can be detrimental to the developing embryo [ 85 ]. These alterations are mainly studied in mouse neural progenitor cells in the early embryonic stage.…”

Section: Epigenetic Effects Of Early Paementioning

confidence: 99%

The Effects of Early Prenatal Alcohol Exposure on Epigenome and Embryonic Development

Wallén

Auvinen

Kaminen‐Ahola

2021

Genes

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Prenatal alcohol exposure is one of the most significant causes of developmental disability in the Western world. Maternal alcohol consumption during pregnancy leads to an increased risk of neurological deficits and developmental abnormalities in the fetus. Over the past decade, several human and animal studies have demonstrated that alcohol causes alterations in epigenetic marks, including DNA methylation, histone modifications, and non-coding RNAs. There is an increasing amount of evidence that early pregnancy is a sensitive period for environmental-induced epigenetic changes. It is a dynamic period of epigenetic reprogramming, cell divisions, and DNA replication and, therefore, a particularly interesting period to study the molecular changes caused by alcohol exposure as well as the etiology of alcohol-induced developmental disorders. This article will review the current knowledge about the in vivo and in vitro effects of alcohol exposure on the epigenome, gene regulation, and the phenotype during the first weeks of pregnancy.

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“…Although several environmental factors are known to increase the prevalence of CL and/or CP in humans and mice, it is still unclear how these factors disturb cellular events that are crucial for craniofacial development. It is known that the expression of microRNAs (miRs), which are short (around 22 nucleotides) non‐coding RNAs that act as post‐transcriptional regulators of their target genes, can be altered by environmental factors 95,96 . Pre‐miRs are transcribed from their coding genes, which are located at either a non‐protein‐coding region or a protein‐coding region, and processed by Drosha (pri‐miRs to pre‐miRs) and Dicer (pre‐miRs to mature miRs) to mature miRs.…”

Section: Pathological Mechanisms Of Cleft Palatementioning

confidence: 99%

Gene–environment interplay and MicroRNAs in cleft lip and cleft palate

Iwata

2020

Oral Science International

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Cleft lip (CL) with/without cleft palate (CP) (hereafter CL/P) is the second most common congenital birth defect, affecting 7.94 to 9.92 children per 10 000 live births worldwide, followed by Down syndrome. An increasing number of genes have been identified as affecting susceptibility and/or as causative genes for CL/P in mouse How to cite this article: IwataJ. Gene-environment interplay and MicroRNAs in cleft lip and cleft palate.

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Maternal alcohol consumption and altered miRNAs in the developing fetus: Context and future perspectives

Cited by 23 publications

References 48 publications

MicroRNA-374a, -4680, and -133b suppress cell proliferation through the regulation of genes associated with human cleft palate in cultured human palate cells

MicroRNA-374a, -4680, and -133b suppress cell proliferation through the regulation of genes associated with human cleft palate in cultured human palate cells

The Effects of Early Prenatal Alcohol Exposure on Epigenome and Embryonic Development

Gene–environment interplay and MicroRNAs in cleft lip and cleft palate

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