Project description:Bronchopulmonary dysplasia (BPD) is the major cause of chronic lung disease (CLD) and morbidity in preterm infants, which characterized by impaired pulmonary alveolar development in preterm infants. There is increasing evidence that micro RNA (miRNA) has a close association with the development of pulmonary diseasesincluding lung growth, pulmonary fibrosis, pneumonia, etc. The potential role of miRNA in the pathogenesis of BPD is unclear. This study aims to clarify the role of adrenomedullin (ADM) regulated by miRNA-547-3p during the process of BPD and illustrate the protective effect of ADM involved in preterm infants.We indentified the differential expressed miRNA and their potential target genes, microarray analysis using Agilent Human 4x44K Gene Expression Microarrays v2 and miRCURY LNA™ microRNA Array was performed. The results of miRNA chip were scanned by Axon GenePix 4000B and the signal of probes were read by GenePix Pro 6.0 software. Only the target genes which exist in both two databases and having different expression trend were remained. Thus, miRNA-574-3p and it’s target gene ADM were selected to do the further research in our study. And we verified miRNA-574-3p and ADM expression in BPD premature infants by realtime q-PCR. After the microarray expression analysis, there were 516 probes differential expressed between BPD samples and normal samples. Among them, 510 were up-regulated and 213 were down-regulated. Meanwhile, to the miRNA aspect, there were 37 up-regulated and 44 down-regulated. After text mining, we found ADM was already found play a role in BPD. ADM is an endogenous peptide with potent angiogenic, anti-oxidant, and anti-inflammatory properties. Realtime q-PCR assay results showed that, miRNA-574-3p expression level in blood samples from preterm infants with BPD was significantly decreased, ADM expression level in blood samples from preterm infants with BPD was significantly increased. In our study, we found that up-regulation of ADM regulated by miRNA-574-3p could protect preterm infants with BPD. These data provide novel insights into ADM regulated by miRNA-574-3p which may be shed light on BPD prevention and treatment.
Project description:Bronchopulmonary dysplasia (BPD) is the major cause of chronic lung disease (CLD) and morbidity in preterm infants, which characterized by impaired pulmonary alveolar development in preterm infants. There is increasing evidence that micro RNA (miRNA) has a close association with the development of pulmonary diseasesincluding lung growth, pulmonary fibrosis, pneumonia, etc. The potential role of miRNA in the pathogenesis of BPD is unclear. This study aims to clarify the role of adrenomedullin (ADM) regulated by miRNA-547-3p during the process of BPD and illustrate the protective effect of ADM involved in preterm infants.We indentified the differential expressed miRNA and their potential target genes, microarray analysis using Agilent Human 4x44K Gene Expression Microarrays v2 and miRCURY LNA™ microRNA Array was performed. The results of miRNA chip were scanned by Axon GenePix 4000B and the signal of probes were read by GenePix Pro 6.0 software. Only the target genes which exist in both two databases and having different expression trend were remained. Thus, miRNA-574-3p and it’s target gene ADM were selected to do the further research in our study. And we verified miRNA-574-3p and ADM expression in BPD premature infants by realtime q-PCR. After the microarray expression analysis, there were 516 probes differential expressed between BPD samples and normal samples. Among them, 510 were up-regulated and 213 were down-regulated. Meanwhile, to the miRNA aspect, there were 37 up-regulated and 44 down-regulated. After text mining, we found ADM was already found play a role in BPD. ADM is an endogenous peptide with potent angiogenic, anti-oxidant, and anti-inflammatory properties. Realtime q-PCR assay results showed that, miRNA-574-3p expression level in blood samples from preterm infants with BPD was significantly decreased, ADM expression level in blood samples from preterm infants with BPD was significantly increased. In our study, we found that up-regulation of ADM regulated by miRNA-574-3p could protect preterm infants with BPD. These data provide novel insights into ADM regulated by miRNA-574-3p which may be shed light on BPD prevention and treatment.
Project description:BackgroundSchizophrenia (SCZ) is a severe neurodevelopmental disorder with brain dysfunction. This study aimed to use bioinformatic analysis to identify candidate blood biomarkers for SCZ.MethodsThe study collected peripheral blood leukocyte samples of 9 SCZ patients and 20 healthy controls for RNA sequencing analysis. Bioinformatic analyses included differentially expressed genes (DEGs) analysis, pathway enrichment analysis, and weighted gene co-expression network analysis (WGCNA).ResultsThis study identified 1,205 statistically significant DEGs, of which 623 genes were upregulated and 582 genes were downregulated. Functional enrichment analysis showed that DEGs were mainly enriched in cell chemotaxis, cell surface, and serine peptidase activity, as well as involved in Natural killer cell-mediated cytotoxicity. WGCNA identified 16 gene co-expression modules, and five modules were significantly correlated with SCZ (p < 0.05). There were 106 upregulated genes and 90 downregulated genes in the five modules. The top ten genes sorted by the Degree algorithm were RPS28, BRD4, FUS, PABPC1, PCBP1, PCBP2, RPL27A, RPS21, RAG1, and RPL27. RAG1 and the other nine genes belonged to the turquoise and pink module respectively. Pathway enrichment analysis indicated that these 10 genes were mainly involved in processes such as Ribosome, cytoplasmic translation, RNA binding, and protein binding.ConclusionThis study finds that the gene functions in key modules and related enrichment pathways may help to elucidate the molecular pathogenesis of SCZ, and the potential of key genes to become blood biomarkers for SCZ warrants further validation.
Project description:STUDY OBJECTIVE:A close association between the human leukocyte antigen (HLA)-DRB1*1501/DQB1*0602 and abnormalities in some inflammatory cytokines have been demonstrated in narcolepsy. Specific alterations in the immune system have been suggested to occur in this disorder. We attempted to identify alterations in gene expression underlying the abnormalities in the blood cells of narcoleptic patients. DESIGNS:Total RNA from 12 narcolepsy-cataplexy patients and from 12 age- and sex-matched healthy controls were pooled. The pooled samples were initially screened for candidate genes for narcolepsy by differential display analysis using annealing control primers (ACP). The second screening of the samples was carried out by semiquantitative PCR using gene-specific primers. Finally, the expression levels of the candidate genes were further confirmed by quantitative real-time PCR using a new set of samples (20 narcolepsy-cataplexy patients and 20 healthy controls). RESULTS:The second screening revealed differential expression of 4 candidate genes. Among them, MX2 was confirmed as a significantly down-regulated gene in the white blood cells of narcoleptic patients by quantitative real-time PCR. CONCLUSION:We found the MX2 gene to be significantly less expressed in comparison with normal subjects in the white blood cells of narcoleptic patients. This gene is relevant to the immune system. Although differential display analysis using ACP technology has a limitation in that it does not help in determining the functional mechanism underlying sleep/wakefulness dysregulation, it is useful for identifying novel genetic factors related to narcolepsy, such as HLA molecules. Further studies are required to explore the functional relationship between the MX2 gene and narcolepsy pathophysiology.