scholarly journals Identification of novel target genes in human lung tissue involved in chronic obstructive pulmonary disease

2018 ◽  
Vol Volume 13 ◽  
pp. 2255-2259 ◽  
Author(s):  
Lena Heinbockel ◽  
Sebastian Marwitz ◽  
Andra Schromm ◽  
Henrik Watz ◽  
Christian Kugler ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Target Genes ◽  
Human Lung ◽  
Chronic Obstructive ◽  
Human Lung Tissue ◽  
Obstructive Pulmonary Disease ◽  
Novel Target

Proteomics of Human Lung Tissue Identifies Surfactant Protein A as a Marker of Chronic Obstructive Pulmonary Disease

2008 ◽  
Vol 7 (12) ◽  
pp. 5125-5132 ◽  
Author(s):  
Steffen Ohlmeier ◽  
Minna Vuolanto ◽  
Tuula Toljamo ◽  
Katri Vuopala ◽  
Kaisa Salmenkivi ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Human Lung ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Chronic Obstructive ◽  
Human Lung Tissue ◽  
Obstructive Pulmonary Disease

scholarly journals Whole transcriptome analyis of human lung tissue to identify COPD-associated gene

2020 ◽  
Author(s):  
Yizhang Zhu ◽  
Qiuyu Li ◽  
Aiyuan Zhou ◽  
Alexandra C. Racanelli ◽  
Augustine M.K. Choi ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Human Lung ◽  
R Package ◽  
Tissue Expression ◽  
Chronic Obstructive ◽  
Common Disease ◽  
Human Lung Tissue ◽  
Obstructive Pulmonary Disease

Abstract Background: Chronic obstructive pulmonary disease (COPD) is a common disease characterized by persistent respiratory symptoms and airflow restriction. The mechanisms underlying pathogenesis in COPD are still poorly understood. Identification of the dysfunctional genes in human lung from patients with Chronic obstructive pulmonary disease (COPD) will help up to understand the pathology of this disease. To identify the dysfunctional genes in human lung from patients with Chronic obstructive pulmonary disease (COPD). We used transcriptomic data of lung tissue for 91 COPD cases and 182 matched healthy controls from the Genotype-Tissue Expression (GTEx) database. We employed a stringent model controlling for known covariates and hidden confounders. DESeq2 R package (v1.20.0) was used to test for differential expression.Results: We identified 1,359 significant differentially expressed genes (DEG) with 707 upregulated and 602 downregulated respectively. We evaluated the identified DEGs in an independent microarray cohort of 219 COPD and 108 controls, demonstrating the robustness of our result. Functional annotation of COPD-associated genes highlighted the activation of complement cascade, dysregulation of inflammatory response and extracellular matrix organization in the COPD patients. In addition, we identified several novel key-hub genes involved in the COPD pathogenesis using a network analysis method.Conclusion: In summary, our study represents the comprehensive analysis of gene expression on COPD with the largest sample size, providing great resource for the molecular research in the COPD community.

scholarly journals Whole transcriptome analysis of human lung tissue to identify COPD-associated gene

2020 ◽  
Author(s):  
Qiuyu Li ◽  
Yizhang Zhu ◽  
Aiyuan Zhou ◽  
Yuxin Yin
Keyword(s):  
Lung Tissue ◽  
Human Lung ◽  
Tissue Expression ◽  
Chronic Obstructive ◽  
Human Lung Tissue ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Matrix Organization ◽  
Whole Transcriptome Analysis ◽  
Whole Transcriptome

Abstract Identification of the dysfunctional genes in human lung from patients with Chronic obstructive pulmonary disease (COPD) will help up to understand the pathology of this disease. Here, using transcriptomic data of lung tissue for 91 COPD cases and 182 matched healthy controls from the Genotype-Tissue Expression (GTEx) database. Employing a stringent model controlling for known covariates and hidden confounders, we identified 1,359 significant differentially expressed genes (DEG) with 707 upregulated and 602 downregulated respectively. We evaluated the identified DEGs in an independent microarray cohort of 219 COPD and 108 controls, demonstrating the robustness of our result. Functional annotation of COPD-associated genes highlighted the activation of complement cascade, dysregulation of inflammatory response and extracellular matrix organization in the COPD patients. In addition, we identified several novel key-hub genes involved in the COPD pathogenesis using a network analysis method. In summary, our study represents the comprehensive analysis of gene expression on COPD with the largest sample size providing great resource for the molecular research in the COPD community.

scholarly journals CUL1-Mediated Organelle Fission Pathway Inhibits the Development of Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Ran Li ◽  
Feng Xu ◽  
Xiao Wu ◽  
Shaoping Ji ◽  
Ruixue Xia
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Transcription Factors ◽  
Pulmonary Disease ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Development Trend ◽  
Chronic Obstructive ◽  
Hypergeometric Test ◽  
Obstructive Pulmonary Disease ◽  
Depth Analysis

Chronic obstructive pulmonary disease (COPD) is a global high-incidence chronic airway inflammation disease. Its deterioration will lead to more serious lung lesions and even lung cancer. Therefore, it is urgent to determine the pathogenesis of COPD and find potential therapeutic targets. The purpose of this study is to reveal the molecular mechanism of COPD disease development through in-depth analysis of transcription factors and ncRNA-driven pathogenic modules of COPD. We obtained the expression profile of COPD-related microRNAs from the NCBI-GEO database and analyzed the differences among groups to identify the microRNAs significantly associated with COPD. Then, their target genes are predicted and mapped to a protein-protein interaction (PPI) network. Finally, key transcription factors and the ncRNA of the regulatory module were identified based on the hypergeometric test. The results showed that CUL1 was the most interactive gene in the highly interactive module, so it was recognized as a dysfunctional molecule of COPD. Enrichment analysis also showed that it was much involved in the biological process of organelle fission, the highest number of regulatory modules. In addition, ncRNAs, mainly composed of miR-590-3p, miR-495-3p, miR-186-5p, and transcription factors such as MYC, BRCA1, and CDX2, significantly regulate COPD dysfunction blocks. In summary, we revealed that the COPD-related target gene CUL1 plays a key role in the potential dysfunction of the disease. It promotes the proliferation of fibroblast cells in COPD patients by mediating functional signals of organelle fission and thus participates in the progress of the disease. Our research helps biologists to further understand the etiology and development trend of COPD.

Sign in / Sign up

Export Citation Format

Share Document