Perinatal inflammation alters histone 3 and histone 4 methylation patterns: Effects of MiR-29b supplementation

Sugar, Sophia S; Heyob, Kathryn M.; Cheng, Xinwei; Lee, Robert J.; Rogers, Lynette K.

doi:10.1016/j.redox.2020.101783

Cited by 10 publications

(5 citation statements)

References 40 publications

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“…Instead of the cytoplasm, miR-29b has been shown to be transported to the nucleus where it can act as a transcriptional or splicing factor 54 . The whole microRNA-29b family has been named epi-miRNAs, as they are capable of controlling epigenetic landscape by targeting key epigenetic effectors, such as DNA methyltransferases and histone deasetylases 55,56 having longer lasting effects on gene expression. It is also plausible that hsa-miR-29b-3p levels themselves are regulated by pre-and perinatal conditions and/or their consequences as this miRNA has been suggested to have an extensive regulatory role in embryonic development 57,58 .…”

Section: Discussionmentioning

confidence: 99%

Adulthood blood levels of hsa-miR-29b-3p associate with preterm birth and adult metabolic and cognitive health

Marttila

Rovio

Mishra

et al. 2021

Sci Rep

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Preterm birth (PTB) is associated with increased risk of type 2 diabetes and neurocognitive impairment later in life. We analyzed for the first time the associations of PTB with blood miRNA levels in adulthood. We also investigated the relationship of PTB associated miRNAs and adulthood phenotypes previously linked with premature birth. Blood MicroRNA profiling, genome-wide gene expression analysis, computer-based cognitive testing battery (CANTAB) and serum NMR metabolomics were performed for Young Finns Study subjects (aged 34–49 years, full-term n = 682, preterm n = 84). Preterm birth (vs. full-term) was associated with adulthood levels of hsa-miR-29b-3p in a fully adjusted regression model (p = 1.90 × 10–4, FDR = 0.046). The levels of hsa-miR-29b-3p were down-regulated in subjects with PTB with appropriate birthweight for gestational age (p = 0.002, fold change [FC] = − 1.20) and specifically in PTB subjects with small birthweight for gestational age (p = 0.095, FC = − 1.39) in comparison to individuals born full term. Hsa-miR-29b-3p levels correlated with the expressions of its target-mRNAs BCL11A and CS and the gene set analysis results indicated a target-mRNA driven association between hsa-miR-29b-3p levels and Alzheimer's disease, Parkinson's disease, Insulin signaling and Regulation of Actin Cytoskeleton pathway expression. The level of hsa-miR-29b-3p was directly associated with visual processing and sustained attention in CANTAB test and inversely associated with serum levels of VLDL subclass component and triglyceride levels. In conlcusion, adult blood levels of hsa-miR-29b-3p were lower in subjects born preterm. Hsa-miR-29b-3p associated with cognitive function and may be linked with adulthood morbidities in subjects born preterm, possibly through regulation of gene sets related to neurodegenerative diseases and insulin signaling as well as VLDL and triglyceride metabolism.

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Section: Discussionmentioning

confidence: 99%

Adulthood blood levels of hsa-miR-29b-3p associate with preterm birth and adult metabolic and cognitive health

Marttila

Rovio

Mishra

et al. 2021

Sci Rep

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“…One recent study on miRNA 29b using the combined model of intrauterine inflammation induced by LPS and postnatal hyperoxia provided a link between miRNA regulation and histone methylation patterns. While exposure to hyperoxia downregulated both miRNA 29b levels and histone 3 and 4 methylation patterns, nanoparticle delivery of miR-29b on day 3 reverted these changes and partially reversed lung histopathology, with reduced septal wall thickness but unchanged alveolar air space [57]. One further dimension arises from the observed specific epigenetic regulation of genes implicated in cell cycle control, pulmonary vessel formation, vascular remodeling, and mesenchymal stem cell function in female mice, while in male mice, endothelium developmental pathways were specifically altered [58].…”

Section: Gene Regulation and Epigenetic Alterationsmentioning

confidence: 98%

Oxygen Toxicity to the Immature Lung—Part I: Pathomechanistic Understanding and Preclinical Perspectives

Choi

Rekers

Dong

et al. 2021

IJMS

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In utero, the fetus and its lungs develop in a hypoxic environment, where HIF-1α and VEGFA signaling constitute major determinants of further development. Disruption of this homeostasis after preterm delivery and extrauterine exposure to high fractions of oxygen are among the key events leading to bronchopulmonary dysplasia (BPD). Reactive oxygen species (ROS) production constitutes the initial driver of pulmonary inflammation and cell death, altered gene expression, and vasoconstriction, leading to the distortion of further lung development. From preclinical studies mainly performed on rodents over the past two decades, the deleterious effects of oxygen toxicity and the injurious insults and downstream cascades arising from ROS production are well recognized. This article provides a concise overview of disease drivers and different therapeutic approaches that have been successfully tested within experimental models. Despite current studies, clinical researchers are still faced with an unmet clinical need, and many of these strategies have not proven to be equally effective in clinical trials. In light of this challenge, adapting experimental models to the complexity of the clinical situation and pursuing new directions constitute appropriate actions to overcome this dilemma. Our review intends to stimulate research activities towards the understanding of an important issue of immature lung injury.

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“…Moreover, epigenetic mechanisms can interact with each other to affect transcription as evidenced by increased methylation of the promoter and correlative decreased expression of the miR-17~92 cluster following a murine hyperoxia model and whose target Tgf-β’s relationship with OS is mentioned above [ 68 ]. Moreover, methylation of histone 3 and 4 has been described following a perinatal inflammatory exposure model as well as a rescue of the alveolar simplification phenotype following miR-29b supplementation [ 70 ].…”

Section: Epigeneticsmentioning

confidence: 99%

Pathogenesis of Bronchopulmonary Dysplasia: Role of Oxidative Stress from ‘Omics’ Studies

2022

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Bronchopulmonary dysplasia (BPD) remains the most common respiratory complication of prematurity as younger and smaller infants are surviving beyond the immediate neonatal period. The recognition that oxidative stress (OS) plays a key role in BPD pathogenesis has been widely accepted since at least the 1980s. In this article, we examine the interplay between OS and genetic regulation and review ‘omics’ data related to OS in BPD. Data from animal models (largely models of hyperoxic lung injury) and from human studies are presented. Epigenetic and transcriptomic analyses have demonstrated several genes related to OS to be differentially expressed in murine models that mimic BPD as well as in premature infants at risk of BPD development and infants with established lung disease. Alterations in the genetic regulation of antioxidant enzymes is a common theme in these studies. Data from metabolomics and proteomics have also demonstrated the potential involvement of OS-related pathways in BPD. A limitation of many studies includes the difficulty of obtaining timely and appropriate samples from human patients. Additional ‘omics’ studies could further our understanding of the role of OS in BPD pathogenesis, which may prove beneficial for prevention and timely diagnosis, and aid in the development of targeted therapies.

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Perinatal inflammation alters histone 3 and histone 4 methylation patterns: Effects of MiR-29b supplementation

Cited by 10 publications

References 40 publications

Adulthood blood levels of hsa-miR-29b-3p associate with preterm birth and adult metabolic and cognitive health

Adulthood blood levels of hsa-miR-29b-3p associate with preterm birth and adult metabolic and cognitive health

Oxygen Toxicity to the Immature Lung—Part I: Pathomechanistic Understanding and Preclinical Perspectives

Pathogenesis of Bronchopulmonary Dysplasia: Role of Oxidative Stress from ‘Omics’ Studies

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