Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells
Particulate matter (PM) has become the main risk factor for public health, being linked with an increased risk of respiratory diseases. However, the potential mechanisms underlying PM-induced lung injury have not been well elucidated. In this study, we systematically integrated the metabolomics, lip...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-05-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323003433 |
| _version_ | 1797840555815731200 |
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| author | Jian Wang Yingying Zeng Juan Song Mengchan Zhu Guiping Zhu Hui Cai Cuicui Chen Meiling Jin Yuanlin Song |
| author_facet | Jian Wang Yingying Zeng Juan Song Mengchan Zhu Guiping Zhu Hui Cai Cuicui Chen Meiling Jin Yuanlin Song |
| author_sort | Jian Wang |
| collection | DOAJ |
| description | Particulate matter (PM) has become the main risk factor for public health, being linked with an increased risk of respiratory diseases. However, the potential mechanisms underlying PM-induced lung injury have not been well elucidated. In this study, we systematically integrated the metabolomics, lipidomics, and transcriptomics data obtained from the human bronchial epithelial cells (HBECs) exposed to PM to reveal metabolic disorders in PM-induced lung injury. We identified 170 differentially expressed metabolites (82 upregulated and 88 downregulated metabolites), 218 differentially expressed lipid metabolites (125 upregulated and 93 downregulated lipid metabolites), and 1417 differentially expressed genes (643 upregulated and 774 downregulated genes). Seven key metabolites (prostaglandin E2, inosinic acid, L-arginine, L-citrulline, L-leucine, adenosine, and adenosine monophosphate), and two main lipid subclasses (triglyceride and phosphatidylcholine) were identified in PM-exposed HBECs. The amino acid metabolism, lipid metabolism, and carbohydrate metabolism were the significantly enriched pathways of identified differentially expressed genes. Then, conjoint analysis of these three omics data and further qRT-PCR validation showed that arachidonic acid metabolism, glycerolipid metabolism, and glutathione metabolism were the key metabolic pathways in PM-exposed HBECs. The knockout of AKR1C3 in arachidonic acid metabolism or GPAT3 in glycerolipid metabolism could significantly inhibit PM-induced inflammatory responses in HBECs. These results revealed the potential metabolic pathways in PM-exposed HBECs and provided a new target to protect from PM-induced airway damage. |
| first_indexed | 2024-04-09T16:17:16Z |
| format | Article |
| id | doaj.art-a1be69f0e008479893c1358a329fa54c |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-04-09T16:17:16Z |
| publishDate | 2023-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-a1be69f0e008479893c1358a329fa54c2023-04-24T04:36:45ZengElsevierEcotoxicology and Environmental Safety0147-65132023-05-01256114839Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cellsJian Wang0Yingying Zeng1Juan Song2Mengchan Zhu3Guiping Zhu4Hui Cai5Cuicui Chen6Meiling Jin7Yuanlin Song8Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, ChinaDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China; Corresponding author.Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China; Shanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China; Shanghai Institute of Infectious Disease and Biosecurity, Shanghai 200032, China; Shanghai Respiratory Research Institute, Shanghai 200032, China; Corresponding author at: Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China.Particulate matter (PM) has become the main risk factor for public health, being linked with an increased risk of respiratory diseases. However, the potential mechanisms underlying PM-induced lung injury have not been well elucidated. In this study, we systematically integrated the metabolomics, lipidomics, and transcriptomics data obtained from the human bronchial epithelial cells (HBECs) exposed to PM to reveal metabolic disorders in PM-induced lung injury. We identified 170 differentially expressed metabolites (82 upregulated and 88 downregulated metabolites), 218 differentially expressed lipid metabolites (125 upregulated and 93 downregulated lipid metabolites), and 1417 differentially expressed genes (643 upregulated and 774 downregulated genes). Seven key metabolites (prostaglandin E2, inosinic acid, L-arginine, L-citrulline, L-leucine, adenosine, and adenosine monophosphate), and two main lipid subclasses (triglyceride and phosphatidylcholine) were identified in PM-exposed HBECs. The amino acid metabolism, lipid metabolism, and carbohydrate metabolism were the significantly enriched pathways of identified differentially expressed genes. Then, conjoint analysis of these three omics data and further qRT-PCR validation showed that arachidonic acid metabolism, glycerolipid metabolism, and glutathione metabolism were the key metabolic pathways in PM-exposed HBECs. The knockout of AKR1C3 in arachidonic acid metabolism or GPAT3 in glycerolipid metabolism could significantly inhibit PM-induced inflammatory responses in HBECs. These results revealed the potential metabolic pathways in PM-exposed HBECs and provided a new target to protect from PM-induced airway damage.http://www.sciencedirect.com/science/article/pii/S0147651323003433Particulate matterMetabolomicsLipidomicsTranscriptomicsMulti-omics |
| spellingShingle | Jian Wang Yingying Zeng Juan Song Mengchan Zhu Guiping Zhu Hui Cai Cuicui Chen Meiling Jin Yuanlin Song Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells Ecotoxicology and Environmental Safety Particulate matter Metabolomics Lipidomics Transcriptomics Multi-omics |
| title | Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells |
| title_full | Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells |
| title_fullStr | Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells |
| title_full_unstemmed | Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells |
| title_short | Perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter-induced inflammatory responses in human bronchial epithelial cells |
| title_sort | perturbation of arachidonic acid and glycerolipid metabolism promoted particulate matter induced inflammatory responses in human bronchial epithelial cells |
| topic | Particulate matter Metabolomics Lipidomics Transcriptomics Multi-omics |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323003433 |
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