scholarly journals Faculty Opinions recommendation of Gene expression profiles distinguish idiopathic pulmonary fibrosis from hypersensitivity pneumonitis.

Author(s):  
Yvon Cormier
2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Ning Zhang ◽  
Yali Guo ◽  
Cong Wu ◽  
Bohan Jiang ◽  
Yuguang Wang

Background. Idiopathic Pulmonary Fibrosis (IPF) is one of the most common idiopathic interstitial pneumonia, which can occur all over the world. The median survival time of patients is about 3-5 years, and the mortality is relatively high. Objective. To reveal the potential molecular characteristics of IPF and deepen the understanding of the molecular mechanism of IPF. In order to provide some guidance for the clinical treatment, new drug development, and prognosis judgment of IPF. Although the preliminary conclusion of this study has certain guiding significance for the treatment of IPF and so on, it needs more accurate analytical approaches and large sample clinical trials to verify. Methods. 220 patients with IPF were divided into different subgroups according to the gene expression profiles, which were obtained from the Gene Expression Omnibus (GEO) database. In addition, these subgroups present different expression forms and clinical features. Therefore, weighted gene coexpression analysis (WGCNA) was used to seek the differences between subtypes. And six subgroup-specific WGCNA modules were identified. Results. Combined with the characteristics of WGCNA and KEGG enrichment modules, the autophagic pathway was only upregulated in subgroup I and enriched significantly. The differentiation pathways of Th1 and Th2 cells were only upregulated and enriched in subgroup II. At the same time, combined with clinical information, IPF patients in subgroup II were older and more serious, which may be closely related to the differentiation of Th1 and Th2 cells. In contrast, the neuroactive ligand-receptor interaction pathway and Ca+ signaling pathway were significantly upregulated and enriched in subgroup III. Although there was no significant difference in prognosis between subgroup I and subgroup III, their intrinsic biological characteristics were very different. These results suggest that the subtypes may represent risk factors of age and intrinsic biological characteristics and may also partly reflect the severity of the disease. Conclusion. In conclusion, current studies have improved our understanding of IPF-related molecular mechanisms. At the same time, because the results show that patients from different subgroups may have their own unique gene expression patterns, it reminds us that patients in each subgroup should receive more personalized treatment.


2009 ◽  
Vol 180 (2) ◽  
pp. 167-175 ◽  
Author(s):  
Kazuhisa Konishi ◽  
Kevin F. Gibson ◽  
Kathleen O. Lindell ◽  
Thomas J. Richards ◽  
Yingze Zhang ◽  
...  

2020 ◽  
Vol 318 (4) ◽  
pp. L684-L697 ◽  
Author(s):  
Valentina Biasin ◽  
Slaven Crnkovic ◽  
Anita Sahu-Osen ◽  
Anna Birnhuber ◽  
Elie El Agha ◽  
...  

Pulmonary fibrosis is characterized by pronounced collagen deposition and myofibroblast expansion, whose origin and plasticity remain elusive. We utilized a fate-mapping approach to investigate α-smooth muscle actin (αSMA)+ and platelet-derived growth factor receptor α (PDGFRα)+ cells in two lung fibrosis models, complemented by cell type-specific next-generation sequencing and investigations on human lungs. Our data revealed that αSMA+ and PDGFRα+ cells mark two distinct mesenchymal lineages with minimal transdifferentiation potential during lung fibrotic remodeling. Parenchymal and perivascular fibrotic regions were populated predominantly with PDGFRα+ cells expressing collagen, while αSMA+ cells in the parenchyma and vessel wall showed variable expression of collagen and the contractile protein desmin. The distinct gene expression profile found in normal conditions was retained during pathologic remodeling. Cumulatively, our findings identify αSMA+ and PDGFRα+ cells as two separate lineages with distinct gene expression profiles in adult lungs. This cellular heterogeneity suggests that anti-fibrotic therapy should target diverse cell populations.


2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Fan Wang ◽  
Pei Li ◽  
Feng-sen Li

Idiopathic pulmonary fibrosis (IPF), the most frequent form of irreversible interstitial pneumonia with unknown etiology, is characterized by massive remodeling of lung architecture and followed by progressive loss of lung function. However, the key regulatory genes and the specific signaling pathways involved in the onset and progression of IPF still remain unclear. The present study is aimed at investigating the key role of long noncoding RNAs (lncRNAs) and transcription factors (TFs) involved in the pathogenesis of IPF through the integrated analysis of three gene expression profiles from the GEO dataset (GSE2052, GSE44723, and GSE24206). A total of 8483 differentially expressed genes (DEGs) including 988 upregulated and 7495 downregulated genes were filtered. Subsequently, following the intersection of these DEGs, 29 overlapping genes were identified and further analyzed using a bioinformatics approach. Furthermore, the protein-protein interaction (PPI) network was used to obtain 18 modules of related genes. The hub genes were identified through hypergeometric testing, which were closely associated with ubiquitin-mediated proteolysis, the spliceosome, and the cell cycle. The significant difference was observed in the expression of these key genes, such as lncRNA MALAT1, E2F1, and YBX1, in the peripheral blood of IPF patients when compared with those normal control subjects by real-time polymerase chain reaction (RT-PCR) analysis. This study indicated that lncRNA MALAT1, E2F1, and YBX1 may be key regulators for the pathogenesis of IPF.


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