Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or . mil. Before sharing sensitive information, make sure you’re on a federal government site VSports app下载. .

Https

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. V体育官网.

. 2020 May 26:2020:5390107.
doi: 10.1155/2020/5390107. eCollection 2020.

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

Ran Li  1 , Feng Xu  2 , Xiao Wu  2 , Shaoping Ji  3 , Ruixue Xia  2
Affiliations

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

Ran Li et al. Comput Math Methods Med. .

Abstract

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. VSports手机版.

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Highly interactive module characterizes 19 COPD highly interactive modules obtained from modular analysis of potential dysfunction of COPD. Different color circle dot groups represent 19 different module genes, and the center yellow dot group represents module overlap genes.
Figure 2
Figure 2
Functional and pathway enrichment analysis of modular genes (excerpts). (a). GO functional enrichment analysis of module genes. From blue to purple, the enrichment increased dramatically. The larger the circle, the larger the proportion of module genes in GO functional entry genes. (b). KEGG pathway enrichment analysis of modular genes. From blue to purple, the enrichment increased markedly. The larger the circle, the larger the proportion of module genes to KEGG pathway entry genes. (c). Network map of the functional pathway.
Figure 3
Figure 3
Highly interactive module-driven genes. Node colors from brown to dark red represent the connectivity of module genes from tiny to large, and each node group represents each module.
Figure 4
Figure 4
Regulation of the ncRNA pivot regulator on the dysfunction module. The green circle represents the module, the blue circle represents the ncRNA of the control module, and the circle size represents the number of control modules. The larger the circle, the more the number of regulations.
Figure 5
Figure 5
Regulation of the TF pivot regulator on the dysfunction module. The brown square represents the module. The blue square represents the transcription factor of the regulatory module.
See this image and copyright information in PMC

References

    1. Makris S., Johnston S. Recent advances in understanding rhinovirus immunity. F1000Research. 2018;7 doi: 10.12688/f1000research.15337.1. - DOI - PMC - PubMed
    1. Su Y. C., Jalalvand F., Thegerström J., Riesbeck K. The interplay between immune response and bacterial infection in COPD: focus upon non-typeable Haemophilus influenzae. Frontiers in Immunology. 2018;9 doi: 10.3389/fimmu.2018.02530. - DOI (V体育官网入口) - PMC - PubMed
    1. Pires N., Pinto P., Marçal N., et al. Pharmacological treatment of COPD – New evidence. Pulmonology. 2019;25(2):90–96. doi: 10.1016/j.pulmoe.2018.10.005. - DOI - PubMed
    1. Wang H., Anthony D., Selemidis S., Vlahos R., Bozinovski S. Resolving viral-induced secondary bacterial infection in COPD: a concise review. Frontiers in Immunology. 2018;9:p. 2345. doi: 10.3389/fimmu.2018.02345. - DOI - PMC - PubMed
    1. van der Leest S., Duiverman M. L. High-intensity non-invasive ventilation in stable hypercapnic COPD: evidence of efficacy and practical advice. Respirology. 2019;24(4):318–328. doi: 10.1111/resp.13450. - DOI - PubMed

MeSH terms