MicroRNA-mRNA interactions in a murine model of hyperoxia-induced bronchopulmonary dysplasia

Dong, Jie; Carey, William A.; Abel, Stuart; Collura, Christopher A.; Jiang, Guoqian; Tomaszek, Sandra; Sutor, Shari L.; Roden, Anja C.; Asmann, Yan W.; Prakash, Y. S.; Wigle, Dennis A.

doi:10.1186/1471-2164-13-204

Cited by 69 publications

(44 citation statements)

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“…According to the inclusion criteria and identification of duplicate publications, only three independent studies (Zhang et al, 2011;Dong et al, 2012;Bhaskaran et al, 2012) were ultimately included in the analysis. The characteristics of these studies are listed in Table 1 in the order of publication date.…”

Section: Independent Studies Includedmentioning

confidence: 99%

“…Furthermore, they also provided detailed accounts of miRNA expression during lung development in BPD. Dong et al (2012) compared miRNA profiles at P14 and P29 between BPD and control groups. In addition, they listed possible target genes of the differentially expressed miRNAs using mRNA array analysis.…”

Section: Independent Studies Includedmentioning

confidence: 99%

“…Differentially expressed miRNAs during lung development with BPD Zhang et al (2011) screened 36 specific microRNAs that showed aberrant regulation in the lung development of BPD mice only, and Dong et al (2012) showed an intersection of dynamically regulated miRNAs in normal lung alveolar development and hyperoxia-induced BPD. To ensure accuracy and comparability of these two studies, we also investigated the intersection for the miRNA sets between normal lung development and BPD lung tissues based on original data of Zhang et al (2011).…”

Section: Differentially Expressed Mirnas Between Bpd and Control Groupsmentioning

confidence: 99%

“…Based on the basic regulating mechanism of miRNA, at the post-transcription level, down-regulated miRNAs generally leads to up-regulation in expression of targeted genes and vice versa. Similarly, Dong et al (2012) also used an mRNA array to profile the expression of target genes, and then performed a Gene Ontology analysis to determine the biological process of BPD. In order to identify target genes of differentially expressed miRNAs, an intersection of two databases (miRBase and TargetScan) was also conducted in their study (Tables 5 and 6).…”

Section: Differentially Expressed Mirnas Between Bpd and Control Groupsmentioning

confidence: 99%

“…Therefore, microarray-based miRNA profiling assays have attracted increasing attention because they constitute an efficient methodology for parallel screening of the expression of hundreds of miRNAs using a high-throughput probe. With the aim of identifying meaningful miRNAs of BPD, over the past several years some investigators have carried out miRNAs expression profiling studies in mammalian lung tissues (Zhang et al, 2011;Dong et al, 2012;Bhaskaran et al, 2012). As a result, dozens of differentially expressed miRNAs have been identified.…”

Section: Introductionmentioning

confidence: 99%

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

Yang

Qiu²,

Kan³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Over the past several years, several microRNA (miRNA) expression profiling studies have been carried out on bronchopulmonary dysplasia (BPD) in mammalian lung tissues. The most effective way to identify these important miRNAs is to systematically search for similar signatures identified in multiple independent studies. Accordingly, a meta-analysis was conducted to review published miRNA expression profiling studies that compared miRNA expression profiles between BPD lung tissues and normal lung tissues. A vote-counting strategy that considered the total number of studies and time points reporting differential expression was applied. Furthermore, cut-off criteria of statistically significant differentially expressed miRNAs as defined by the author and their predicted target genes, if available, as well as the list of up-and down-regulated miRNA features, were collected and recorded. Results of the meta-analysis revealed that 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 groups. 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 not only in the process of normal lung development, but also during the progress of BPD. Finally, several meaningful target genes (such as the HPGD and NTRK genes) of common miRNAs (such as miRNA-21 and miRNA-141) were systematically predicted. These specific miRNAs may provide clues of the potential mechanisms involved in BPD. Further mechanistic and external validation studies are needed to confirm the clinical significance of these miRNAs in the development of BPD.

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Section: Independent Studies Includedmentioning

confidence: 99%

Section: Independent Studies Includedmentioning

confidence: 99%

Section: Differentially Expressed Mirnas Between Bpd and Control Groupsmentioning

confidence: 99%

Section: Differentially Expressed Mirnas Between Bpd and Control Groupsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Yang

Qiu²,

Kan³

et al. 2013

Genet. Mol. Res.

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MicroRNA‐421 inhibition alleviates bronchopulmonary dysplasia in a mouse model via targeting Fgf10

Yuan

Daiqun

Huang

et al. 2019

J of Cellular Biochemistry

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Bronchopulmonary dysplasia (BPD) is a common and refractory disease affecting newborn children and infants with alveolar dysplasia and declined pulmonary function. Several microRNAs (miRNAs) have been found to be differentially expressed in BPD progression. This study further explores the role of miR‐421 via fibroblast growth factor 10 (Fgf10) in mice with BPD. A mouse model of BPD was established through the induction of hyperoxia, in which the expression pattern of miR‐421 and Fgf10 was identified. Furthermore, adenovirus‐packed vectors were injected in mice to intervene miR‐421 and Fgf10 expression, including miR‐421 mimics or inhibitors, and si‐Fgf10 to explore the role of miR‐421 and Fgf10 in BPD. The target relationship between miR‐421 and Fgf10 was investigated. Inflammatory response and cell apoptosis were observed in the mice, with inflammatory cytokines and apoptosis‐related factors detected by applying Reverse transcription quantitative polymerase chain reaction, Western blot analysis, and enzyme‐linked immunosorbent assay. Fgf10 was confirmed as a target gene of miR‐421. Elevated expression of miR‐421 was evident, while Fgf10 was poorly expressed in BPD. upregulation of miR‐421 and silence of Fgf10 aggravated inflammatory response in lung tissue and promoted lung cell apoptosis in BPD. The aforementioned alterations could be reversed by downregulation of miR‐421. Collectively, inhibition of miR‐421 can assist in the development of BPD in mice BPD by upregulating Fgf10. Therefore, the present study provides a probable target for the treatment of BPD.

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Circ‐ECH1 May Compete With miR‐708‐5p to Regulate Ntrk2 in Bronchopulmonary Dysplasia

Cheng,

Li,

Tang

et al. 2024

J of Cellular Biochemistry

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Bronchopulmonary dysplasia (BPD) affects patients' quality of life. Circular RNAs participated in BPD. However, circ‐ECH1's role in BPD has not been reported yet. This study aimed to explore the role and mechanism of circ‐ECH1 in BPD. Hyperoxia‐treated type II alveolar epithelial cells (L2 cells) were used as the in vitro BPD model. CCK‐8, flow cytometry, and reactive oxygen species (ROS) were used to evaluate cell viability. Fluorescence in situ hybridization confirmed the subcellular localization. Circ‐ECH1 overexpression (or inhibited) and miR‐708‐5p mimics were used to investigate the roles of circ‐ECH1 and miR‐708‐5p in BPD. Quantitative reverse‐transcription polymerase reaction (qRT‐PCR) detected the expressions of circ‐ECH1, miR‐708‐5p, and neurotrophic receptor tyrosine kinase 2 (Ntrk2). Ntrk2 expression was evaluated by Western blot analysis. Changes in lung tissues were evaluated by hematoxylin and eosin staining. Pulmonary fibrosis was examined by Mason staining. TUNEL staining was performed to evaluate cell apoptosis in lung tissues. RNA sequencing was performed in the lung tissues of BPD rats. The binding between circ‐ECH1 and miR‐708‐5p was confirmed through dual luciferase activity. Hyperoxia reduced cell viability and increased cell apoptosis and ROS accumulation. In addition, hyperoxia decreased the expression levels of circ‐ECH1, which is mainly located in the cytoplasm. Circ‐ECH1 overexpression increased cell viability but reduced cell apoptosis and ROS accumulation. On the contrary, interference with circ‐ECH1 further promoted cell apoptosis and reduced cell activity. Furthermore, circ‐ECH1 overexpression reduced the incidence of pulmonary fibrosis and lung cell apoptosis. RNA sequencing, followed by qRT‐PCR, confirmed that the expressions of Ntrk2 and miR‐708‐5p were affected by circ‐ECH1. miR‐708‐5p mimics reversed the role of circ‐ECH1 in the BPD. Mechanistically, circ‐ECH1 may bind with miR‐708‐5p to regulate Ntrk2 expression. Circ‐ECH1 may compet with miR‐708‐5p to regulate Ntrk2 expression in BPD. The findings provided a new target for BPD treatment.

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MicroRNA-mRNA interactions in a murine model of hyperoxia-induced bronchopulmonary dysplasia

Cited by 69 publications

References 50 publications

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

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

MicroRNA‐421 inhibition alleviates bronchopulmonary dysplasia in a mouse model via targeting Fgf10

Circ‐ECH1 May Compete With miR‐708‐5p to Regulate Ntrk2 in Bronchopulmonary Dysplasia

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