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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Wang, Ruiying Xu, Jianying Wei, Shuang Liu, Xiansheng |
| Abstract | Background Chronic obstructive pulmonary disease (COPD) is a complex respiratory condition influenced by environmental and genetic factors. Using next-generation sequencing, we aimed to identify dysregulated genes and potential therapeutic targets for COPD. Methods Peripheral blood leukocyte RNA profiles from COPD patients and healthy controls were analyzed using next-generation sequencing. Key genes involved in COPD pathogenesis were identified through protein–protein interaction network analysis. In vitro, bronchial epithelial cells treated with cigarette smoke extract (CSE) were used to study the effects on gene expression, cell viability, apoptosis, and ferroptosis. Additionally, Lipocalin 2 (LCN2) inhibition experiments were conducted to elucidate its role in COPD-related cellular processes. Results Analysis of RNA profiles revealed consistent downregulation of 17 genes and upregulation of 21 genes across all COPD groups. Among these, Cathelicidin Antimicrobial Peptide(CAMP), Defensin Alpha 4(DEFA4), Neutrophil Elastase(ELANE), LCN2 and Lactotransferrin(LTF) were identified as potentially important players in COPD pathogenesis. Particularly, LCN2 exhibited a close association with COPD and was found to be involved in cellular processes. In vitro experiments demonstrated that CSE treatment significantly increased LCN2 expression in bronchial epithelial cells in a concentration-dependent manner. Moreover, CSE-induced apoptosis and ferroptosis were observed, along with alterations in cell viability, Glutathione content, Fe2 + accumulation, ROS: Reactive Oxygen Species and Malondialdehyde levels, Lactate Dehydrogenase(LDH) release and Glutathione Peroxidase 4(GPX4) expression. Inhibition of LCN2 expression partially reversed these effects, indicating the pivotal role of LCN2 in COPD-related cellular processes. Conclusion Our study identified six candidate genes: CAMP, DEFA4, ELANE, LCN2, and LTF were upregulated, HSPA1B was downregulated. Notably, LCN2 emerges as a significant biomarker in COPD pathogenesis, exerting its effects by promoting apoptosis and ferroptosis in bronchial epithelial cells. |
| Related Links | https://bmcpulmmed.biomedcentral.com/counter/pdf/10.1186/s12890-024-03357-3.pdf |
| Ending Page | 13 |
| Page Count | 13 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 14712466 |
| DOI | 10.1186/s12890-024-03357-3 |
| Journal | BMC Pulmonary Medicine |
| Issue Number | 1 |
| Volume Number | 24 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2024-10-26 |
| Access Restriction | Open |
| Subject Keyword | Pneumology Respiratory System Internal Medicine Intensive Critical Care Medicine COPD LCN2 Apoptosis Ferroptosis Pneumology/Respiratory System |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pulmonary and Respiratory Medicine |
| Journal Impact Factor | 2.6/2023 |
| 5-Year Journal Impact Factor | 3/2023 |
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