Identification of key pathways and differentially expressed genes in bronchopulmonary dysplasia using bioinformatics analysis

Yan, Weiheng; Jiang, Miaomiao; Zheng, Jun

doi:10.1007/s10529-020-02986-y

Cited by 8 publications

(3 citation statements)

References 41 publications

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“…Angiogenesis and inflammation were considered as important biological changes that contributed to the BPD development, and the expression of interleukin 6 mRNA was observed pronouncedly increased in early BPD. 12 Some potential candidate genes (NOS2, MMP1, CRP, and LBP) in relation to BPD have been discovered in preterm newborns by exome sequencing. 13 The down-regulation of EGR1, JUN, BTG2, and FOS has also been reported to be associated with BPD, and may serve as biomarkers for early BPD diagnosis.…”

Section: Introductionmentioning

confidence: 99%

CD8A is a Promising Biomarker Associated with Immunocytes Infiltration in Hyperoxia-Induced Bronchopulmonary Dysplasia

Du¹,

Zuo²,

Xiong³

et al. 2023

JIR

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Background: Bronchopulmonary dysplasia (BPD) refers to a chronic lung disease which is commonly observed in preterm infants. It can usually be caused by several pathological processes that endanger the long-term lung development, such as inflammation and immune dysfunction. Methods: In this study, a bioinformatics approach was applied to identify the differentially expressed immune-related genes (DEIRGs). We downloaded the transcriptional profiles (GSE32472 dataset) from the Gene Expression Omnibus (GEO) database and performed gene set enrichment analysis (GSEA). Cell type Identification By Estimating Relative Subsets of RNA Transcripts (CIBERSORT), microenvironment cell populations counter (MCPcounter), and Estimation of STromal and Immune cells in Malignant Tumor tissues using Expression data (ESTIMATE) were used for the analysis of the immune cell infiltration landscape of BPD. A weighted co-expression network was subsequently constructed using weighted gene co-expression network analysis (WGCNA) to screen candidate differentially expressed immune related genes (DEIRGs). Results: GSEA results indicated that immune-related pathways were mainly involved in BPD. Ten significantly different immune cell types were observed between BPD and normal groups. A total of 228 DEGs in the turquoise module were identified, and 31 DEIRGs were further identified. Cluster of the differentiation 8 alpha (CD8A) expression was down-regulated in BPD, and its expression was validated by the GSE25286, GSE25293, GSE99633 datasets and qRT-PCR. In addition, CD8A expression was closely associated with immune cells infiltration, especially T cells CD8 and neutrophil. Conclusion: A distinct immune cell infiltration landscape was found between BPD and normal group. CD8A can be a novel candidate biomarker for BPD, which plays an essential role in the onset and progress of hyperoxia-related BPD via the disruption of immune cell functions.

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Section: Introductionmentioning

confidence: 99%

CD8A is a Promising Biomarker Associated with Immunocytes Infiltration in Hyperoxia-Induced Bronchopulmonary Dysplasia

Du¹,

Zuo²,

Xiong³

et al. 2023

JIR

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“…day is the peak). Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are involved in the whole process of acute lung injury and the degradation and remodeling of extracellular matrix in lung injury, and play an important role in the entire pathophysiological process of BPD [16][17][18]. In the physiological process of lung tissue, MMP9 and TIMP1 combine 1:1 to play a normal matrix remodeling effect.…”

Section: Discussionmentioning

confidence: 99%

Study on the mechanism of HE4 in hyperoxia-induced alveolar damage in rats

Yan

Feng

Gao

et al. 2022

Preprint

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Objective: This study investigated the mechanism of human epididymis protein 4 (HE4) in hyperoxia-induced alveolar damage in rats. Methods: The pathological changes of SD rat lung tissue were detected by hematoxylin-eosin staining. Plasma protein levels were measured by enzyme-linked immunosorbent assay (ELISA). The expression of mRNA was detected by real-time RT-PCR. Results: Hyperoxia intervention within 7 days could induce acute lung injury in neonatal SD rats. Hyperoxia induction can increase HE4, MMP9 and TIMP1 in plasma and tissue of neonatal SD rats. By overexpressing and silencing HE4 gene in neonatal rat primary alveolar type II epithelial cells, we found that HE4 protein activates the phosphorylation of ERK and p65, activates the downstream MMP9 signaling pathway, inhibits MMP9 mRNA expression, inhibits protein activity, and reduces COLI degradation, increases collagen secretion, promoting matrix remodeling and fibrosis. Conclusion: HE4 mediates the pathophysiological process of hyperoxia-induced lung injury in rats through ERK, MMP9 and TIMP1 signaling pathways. HE4 overexpression mediates lung basal remodeling and lung injury.

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“…Also, IPA analysis with DE genes suggested increasing arachidonic acid and suppressing Igf1-mediated signaling as causal networks in liver-specific Phb1 +/− , compared with WT. They had in common with downstream targets as Timp1, Scd1, Fdps, and Cyp51a1 (Figure 3), which are mainly associated with the extracellular matrix, fatty acid metabolism, and steroid biosynthesis (Ge et al, 2020;Yan et al, 2020) and downregulated via Mapk14, Srebf1, Stat3, and Insr. This finding is in line with the blocking of activation of phosphoinositide 3kinase by insulin via p38 Mapk in hepatocytes with arachidonic acid (Talukdar et al, 2005) and evidence that arachidonic acid has the potential to decrease insulin-mediated activation of Srebp-1c by inhibiting liver X receptor (Lxr) activation in rat hepatocytes (Chen et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

RNA-Seq Reveals Different Gene Expression in Liver-Specific Prohibitin 1 Knock-Out Mice

Lee

Shouse

et al. 2021

Front. Physiol.

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Prohibitin 1 (PHB1) is an evolutionarily conserved and ubiquitously expressed protein that stabilizes mitochondrial chaperone. Our previous studies showed that liver-specific Phb1 deficiency induced liver injuries and aggravated lipopolysaccharide (LPS)-induced innate immune responses. In this study, we performed RNA-sequencing (RNA-seq) analysis with liver tissues to investigate global gene expression among liver-specific Phb1−/−, Phb1+/−, and WT mice, focusing on the differentially expressed (DE) genes between Phb1+/− and WT. When 78 DE genes were analyzed for biological functions, using ingenuity pathway analysis (IPA) tool, lipid metabolism-related genes, including insulin receptor (Insr), sterol regulatory element-binding transcription factor 1 (Srebf1), Srebf2, and SREBP cleavage-activating protein (Scap) appeared to be downregulated in liver-specific Phb1+/− compared with WT. Diseases and biofunctions analyses conducted by IPA verified that hepatic system diseases, including liver fibrosis, liver hyperplasia/hyperproliferation, and liver necrosis/cell death, which may be caused by hepatotoxicity, were highly associated with liver-specific Phb1 deficiency in mice. Interestingly, of liver disease-related 5 DE genes between Phb1+/− and WT, the mRNA expressions of forkhead box M1 (Foxm1) and TIMP inhibitor of metalloproteinase (Timp1) were matched with validation for RNA-seq in liver tissues and AML12 cells transfected with Phb1 siRNA. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with hepatic Phb1.

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Identification of key pathways and differentially expressed genes in bronchopulmonary dysplasia using bioinformatics analysis

Cited by 8 publications

References 41 publications

CD8A is a Promising Biomarker Associated with Immunocytes Infiltration in Hyperoxia-Induced Bronchopulmonary Dysplasia

CD8A is a Promising Biomarker Associated with Immunocytes Infiltration in Hyperoxia-Induced Bronchopulmonary Dysplasia

Study on the mechanism of HE4 in hyperoxia-induced alveolar damage in rats

RNA-Seq Reveals Different Gene Expression in Liver-Specific Prohibitin 1 Knock-Out Mice

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