MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation
Background: Pulmonary fibrosis (PF) is an irreversible and usually fatal lung disease. In recent years, the therapeutic role of exosomes derived from mesenchymal stem cells (MSC-exos) in anti-fibrotic treatment has received much attention. In this study, we aimed to determine the anti-fibrotic prope...
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Elsevier
2025-01-01
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844024174671 |
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| author | Wei Chen Jie Peng Xiangyi Tang Shao Ouyang |
| author_facet | Wei Chen Jie Peng Xiangyi Tang Shao Ouyang |
| author_sort | Wei Chen |
| collection | DOAJ |
| description | Background: Pulmonary fibrosis (PF) is an irreversible and usually fatal lung disease. In recent years, the therapeutic role of exosomes derived from mesenchymal stem cells (MSC-exos) in anti-fibrotic treatment has received much attention. In this study, we aimed to determine the anti-fibrotic properties and related molecular mechanisms of MSC-exos in Bleomycin(BLM)-induced PF. Methods: We used BLM-induced mice model of PF and in vitro model. MSC-exos were isolated from BMSCs cells using Exo Quick-TC kit and identified using conventional methods. Using cell counting kit-8 (CCK-8) to detect cell viability. Classic molecular biology approaches such as RT-qPCR, Western blot, immunofluorescence, and ELISA were used to examine molecular pathways. Histopathological examination was performed using HE and Masson staining. Results: MSC-exos alleviated inflammation, inhibited epithelial-mesenchymal transition (EMT), and ameliorated PF. Further studies showed that MSC-exos regulated NOD1/NF-kB signaling pathway to suppress the activation of NLRP3 inflammasomes both in vivo and in vitro. Additionally, overexpression of NLRP3 significantly reversed the anti-fibrotic effects of MSC-exos in BLM-induced lung epithelial cells. Conclusion: MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation. |
| format | Article |
| id | doaj-art-68ef4fd5e8d5431f81f4714cf49a6a33 |
| institution | Kabale University |
| issn | 2405-8440 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj-art-68ef4fd5e8d5431f81f4714cf49a6a332025-02-02T05:27:47ZengElsevierHeliyon2405-84402025-01-01112e41436MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammationWei Chen0Jie Peng1Xiangyi Tang2Shao Ouyang3Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, ChinaDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, ChinaDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, ChinaDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of University of South China, Key Laboratory of Heart Failure Prevention & Treatment of Hengyang, Clinical Medicine Research Center of Arteriosclerotic Disease of Hunan Province, Hengyang, Hunan, China; Corresponding author.Background: Pulmonary fibrosis (PF) is an irreversible and usually fatal lung disease. In recent years, the therapeutic role of exosomes derived from mesenchymal stem cells (MSC-exos) in anti-fibrotic treatment has received much attention. In this study, we aimed to determine the anti-fibrotic properties and related molecular mechanisms of MSC-exos in Bleomycin(BLM)-induced PF. Methods: We used BLM-induced mice model of PF and in vitro model. MSC-exos were isolated from BMSCs cells using Exo Quick-TC kit and identified using conventional methods. Using cell counting kit-8 (CCK-8) to detect cell viability. Classic molecular biology approaches such as RT-qPCR, Western blot, immunofluorescence, and ELISA were used to examine molecular pathways. Histopathological examination was performed using HE and Masson staining. Results: MSC-exos alleviated inflammation, inhibited epithelial-mesenchymal transition (EMT), and ameliorated PF. Further studies showed that MSC-exos regulated NOD1/NF-kB signaling pathway to suppress the activation of NLRP3 inflammasomes both in vivo and in vitro. Additionally, overexpression of NLRP3 significantly reversed the anti-fibrotic effects of MSC-exos in BLM-induced lung epithelial cells. Conclusion: MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation.http://www.sciencedirect.com/science/article/pii/S2405844024174671Pulmonary fibrosisMSCExosomeEMTInflammationNLRP3 |
| spellingShingle | Wei Chen Jie Peng Xiangyi Tang Shao Ouyang MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation Heliyon Pulmonary fibrosis MSC Exosome EMT Inflammation NLRP3 |
| title | MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation |
| title_full | MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation |
| title_fullStr | MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation |
| title_full_unstemmed | MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation |
| title_short | MSC-derived exosome ameliorates pulmonary fibrosis by modulating NOD 1/NLRP3-mediated epithelial-mesenchymal transition and inflammation |
| title_sort | msc derived exosome ameliorates pulmonary fibrosis by modulating nod 1 nlrp3 mediated epithelial mesenchymal transition and inflammation |
| topic | Pulmonary fibrosis MSC Exosome EMT Inflammation NLRP3 |
| url | http://www.sciencedirect.com/science/article/pii/S2405844024174671 |
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