MicroRNA expression profiling studies on bronchopulmonary dysplasia: a systematic review and meta-analysis

Yang, Yijun; Qiu, Jianming; Kan, Quan Cheng; Zhou, Xiaoyu; Zhou, Xiaocheng

doi:10.4238/2013.october.30.4

Cited by 37 publications

(23 citation statements)

References 21 publications

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“…Because miRNAs have the ability to modify gene expression rapidly and reversibly, they are ideal mediators for sensing and responding to hypoxic or hyperoxic stress and may therefore be associated with alveolar dysplasias. In a recent analysis by Yang et al 97 , four up-regulated miRNAs (miRNA-21, miRNA-34a, miRNA-431, and Let-7f) and one down-regulated miRNA (miRNA-335) were differentially expressed in BPD lung tissues compared with normal lungs. In addition, eight miRNAs (miRNA-146b, miRNA-29a, miRNA-503, miRNA-411, miRNA-214, miRNA-130b, miRNA-382, and miRNA-181a-1) were found to show differential expression in the process of normal lung development and during the progress of BPD.…”

Section: Biomarkersmentioning

confidence: 96%

Biomarkers, Early Diagnosis, and Clinical Predictors of Bronchopulmonary Dysplasia

Lal

Ambalavanan

2015

Clinics in Perinatology

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Bronchopulmonary Dysplasia (BPD) continues to be an important source of morbidity and mortality in premature neonates. The phenotype of BPD is extremely variable, and diagnosis is a clinical operational definition. A number of clinical and laboratory biomarkers have been proposed for the early identification of infants at higher risk of this disease, to characterize disease activity and severity and for determination of prognosis. Clinical prediction models for BPD have been developed using birth weight, gestational age, indicators of respiratory illness severity, and other clinical variables. Other biomarkers of BPD include those based on imaging of the lungs, lung function measures, and measurements of various analytes in different body fluids (blood, tracheal aspirates, exhaled breath condensates, urine, etc). Novel systems biology ‘omic’ based approaches including but not limited to genomics, proteomics, metabolomics and microbiomics are required for evaluating the multiple interacting cellular and molecular networks that control lung development and injury in BPD. Here we present a critical evaluation of the biomarker approaches studied in the diagnosis of BPD and highlight the future avenues for research in this field.

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Section: Biomarkersmentioning

confidence: 96%

Biomarkers, Early Diagnosis, and Clinical Predictors of Bronchopulmonary Dysplasia

Lal

Ambalavanan

2015

Clinics in Perinatology

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“…In both mice and human lung tissues, DNA methylation, another form of epigenetic regulation, has been shown to alter expression of genes associated with lung development and alveolar septation including a number of genes in angiogenic pathways [75]. Several studies have also shown that epigenetic regulation by microRNA expression is aberrant in BPD [76, 77]. Transgenic miR-150 knockout mice demonstrate increased angiogenesis when exposed to neonatal hyperoxia that may be due to upregulation of glycoprotein non-metastatic melanoma protein B (GPNMB) [78].…”

Section: Introductionmentioning

confidence: 99%

Impaired Pulmonary Vascular Development in Bronchopulmonary Dysplasia

Baker

Abman²

2015

Neonatology

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Bronchopulmonary dysplasia (BPD), the chronic lung disease associated with preterm birth, results from the disruption of normal pulmonary vascular and alveolar growth. Though BPD was once described as primarily due to postnatal injury from mechanical ventilation and oxygen therapy after preterm birth, it is increasingly appreciated that BPD results from antenatal and perinatal factors that interrupt lung development in infants born at the extremes of prematurity. The lung in BPD consists of a simplified parenchymal architecture that limits gas exchange and leads to increased cardiopulmonary morbidity and mortality. This review outlines recent advances in the understanding of pulmonary vascular development and describes how the disruption of these mechanisms results in BPD. We point to future therapies that may augment postnatal vascular growth to prevent and treat this severe chronic lung disease.

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“…Chorioamnionitis may contribute to fetal lung injury and increase the risk of development of bronchopulmonary dysplasia (BPD), a type of neonatal chronic lung disease (2). Changes in microRNA (miRNA) expression have previously been associated with BPD in mouse and rat models and have also been known to play important roles in inflammation and immune response pathways (3)(4)(5). miRNAs are small noncoding RNAs, 18 to 24 nucleotides in length, that regulate the expression of target genes at the posttranscriptional level by binding to their target mRNAs (6).…”

mentioning

confidence: 99%

Choriodecidual Group B Streptococcal Infection Induces miR-155-5p in the Fetal Lung in Macaca nemestrina

et al. 2015

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eThe mechanisms underlying fetal lung injury remain poorly defined. MicroRNAs (miRNAs) are small noncoding, endogenous RNAs that regulate gene expression and have been implicated in the pathogenesis of lung disease. Using a nonhuman primate model of choriodecidual infection, we sought to determine if differentially expressed miRNAs were associated with acute fetal lung injury. After inoculating 10 chronically catheterized pregnant monkeys (Macaca nemestrina) with either group B streptococcus (GBS) at 1 ؋ 10 6 CFU (n ‫؍‬ 5) or saline (n ‫؍‬ 5) in the choriodecidual space, we extracted fetal lung mRNA and miRNA and profiled the changes in expression by microarray analysis. We identified 9 differentially expressed miRNAs in GBS-exposed fetal lungs, but of these, only miR-155-5p was validated by quantitative reverse transcription-PCR (P ‫؍‬ 0.02). Significantly elevated miR-155-5p expression was also observed when immortalized human fetal airway epithelial (FeAE) cells were exposed to proinflammatory cytokines (interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF-␣]). Overexpression of miR-155-5p in FeAE cells in turn increased the production of IL-6 and CXCL10/gamma interferon-induced protein 10, which are implicated in leukocyte recruitment but also in protection from lung injury. Interestingly, while miR-155-5p decreased fibroblast growth factor 9 (FGF9) expression in a luciferase reporter assay, FGF9 levels were actually increased in GBS-exposed fetal lungs in vivo. FGF9 overexpression is associated with abnormal lung development. Thus, upregulation of miR-155-5p may serve as a compensatory mechanism to lessen the increase in FGF9 and prevent aberrant lung development. Understanding the complicated networks regulating lung development in the setting of infection is a key step in identifying how to prevent fetal lung injury leading to bronchopulmonary dysplasia.

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MicroRNA expression profiling studies on bronchopulmonary dysplasia: a systematic review and meta-analysis

Cited by 37 publications

References 21 publications

Biomarkers, Early Diagnosis, and Clinical Predictors of Bronchopulmonary Dysplasia

Biomarkers, Early Diagnosis, and Clinical Predictors of Bronchopulmonary Dysplasia

Impaired Pulmonary Vascular Development in Bronchopulmonary Dysplasia

Choriodecidual Group B Streptococcal Infection Induces miR-155-5p in the Fetal Lung in Macaca nemestrina

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