MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4
Bronchial asthma is characterized by chronic airway inflammation, airway hyperresponsiveness, and airway remodeling. MicroRNA (miRNA) has recently been implicated in the pathogenesis of asthma. However, the mechanisms of different miRNAs in asthma are complicated, and the mechanism of miRNA-182-5p i...
| Main Authors: | , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2022-05-01
|
| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2022.853848/full |
| _version_ | 1818251176958754816 |
|---|---|
| author | Zhiguang Wang Zhiguang Wang Yilan Song Yilan Song Jingzhi Jiang Jingzhi Jiang Yihua Piao Yihua Piao Li Li Li Li Qiaoyun Bai Qiaoyun Bai Chang Xu Chang Xu Hanye Liu Hanye Liu Liangchang Li Liangchang Li Hongmei Piao Hongmei Piao Guanghai Yan Guanghai Yan |
| author_facet | Zhiguang Wang Zhiguang Wang Yilan Song Yilan Song Jingzhi Jiang Jingzhi Jiang Yihua Piao Yihua Piao Li Li Li Li Qiaoyun Bai Qiaoyun Bai Chang Xu Chang Xu Hanye Liu Hanye Liu Liangchang Li Liangchang Li Hongmei Piao Hongmei Piao Guanghai Yan Guanghai Yan |
| author_sort | Zhiguang Wang |
| collection | DOAJ |
| description | Bronchial asthma is characterized by chronic airway inflammation, airway hyperresponsiveness, and airway remodeling. MicroRNA (miRNA) has recently been implicated in the pathogenesis of asthma. However, the mechanisms of different miRNAs in asthma are complicated, and the mechanism of miRNA-182-5p in asthma is still unclear. Here, we aim to explore the mechanism of miRNA182-5p in asthma-related airway inflammation. Ovalbumin (OVA)-induced asthma model was established. MiRNA Microarray Analysis was performed to analyze the differentially expressed miRNAs in the asthma model. We found that the expression of miRNA-182-5p was significantly decreased in OVA-induced asthma. In vitro, IL-13 stimulation of BEAS-2B cells resulted in a significant up-regulation of NOX4 (nicotinamide adenine dinucleotide phosphate oxidase 4), accompanied by mitochondrial damage-induced apoptosis, NLRP3 (NOD-like receptor family pyrin domain-containing 3)/IL-1β activation, and reduced miRNA-182-5p. In contrast, overexpression of miRNA-182-5p significantly inhibited epithelial cell apoptosis and NLRP3/IL-1β activation. In addition, we found that miRNA-182-5p could bind to the 3’ untranscripted region of NOX4 mRNA and inhibit epithelial cell inflammation by reducing oxidative stress and mitochondrial damage. In vivo, miRNA-182-5p agomir treatment significantly reduced the percentage of eosinophils in bronchoalveolar lavage fluid, and down-regulated Th2 inflammatory factors, including IL-4, IL-5, and OVA induced IL-13. Meanwhile, miRNA-182-5p agomir reduced the peribronchial inflammatory cell infiltration, goblet cell proliferation and collagen deposition. In summary, targeting miRNA-182-5p may provide a new strategy for the treatment of asthma. |
| first_indexed | 2024-12-12T16:04:08Z |
| format | Article |
| id | doaj.art-fd17ea0bcbbb4a1ba221df52928b27d1 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-12T16:04:08Z |
| publishDate | 2022-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-fd17ea0bcbbb4a1ba221df52928b27d12022-12-22T00:19:21ZengFrontiers Media S.A.Frontiers in Immunology1664-32242022-05-011310.3389/fimmu.2022.853848853848MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4Zhiguang Wang0Zhiguang Wang1Yilan Song2Yilan Song3Jingzhi Jiang4Jingzhi Jiang5Yihua Piao6Yihua Piao7Li Li8Li Li9Qiaoyun Bai10Qiaoyun Bai11Chang Xu12Chang Xu13Hanye Liu14Hanye Liu15Liangchang Li16Liangchang Li17Hongmei Piao18Hongmei Piao19Guanghai Yan20Guanghai Yan21Jilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Respiratory Medicine, Affiliated Hospital of Yanbian University, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Intensive Care Unit, Affiliated Hospital of Yanbian University, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Respiratory Medicine, Affiliated Hospital of Yanbian University, Yanji, ChinaJilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, ChinaDepartment of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, ChinaBronchial asthma is characterized by chronic airway inflammation, airway hyperresponsiveness, and airway remodeling. MicroRNA (miRNA) has recently been implicated in the pathogenesis of asthma. However, the mechanisms of different miRNAs in asthma are complicated, and the mechanism of miRNA-182-5p in asthma is still unclear. Here, we aim to explore the mechanism of miRNA182-5p in asthma-related airway inflammation. Ovalbumin (OVA)-induced asthma model was established. MiRNA Microarray Analysis was performed to analyze the differentially expressed miRNAs in the asthma model. We found that the expression of miRNA-182-5p was significantly decreased in OVA-induced asthma. In vitro, IL-13 stimulation of BEAS-2B cells resulted in a significant up-regulation of NOX4 (nicotinamide adenine dinucleotide phosphate oxidase 4), accompanied by mitochondrial damage-induced apoptosis, NLRP3 (NOD-like receptor family pyrin domain-containing 3)/IL-1β activation, and reduced miRNA-182-5p. In contrast, overexpression of miRNA-182-5p significantly inhibited epithelial cell apoptosis and NLRP3/IL-1β activation. In addition, we found that miRNA-182-5p could bind to the 3’ untranscripted region of NOX4 mRNA and inhibit epithelial cell inflammation by reducing oxidative stress and mitochondrial damage. In vivo, miRNA-182-5p agomir treatment significantly reduced the percentage of eosinophils in bronchoalveolar lavage fluid, and down-regulated Th2 inflammatory factors, including IL-4, IL-5, and OVA induced IL-13. Meanwhile, miRNA-182-5p agomir reduced the peribronchial inflammatory cell infiltration, goblet cell proliferation and collagen deposition. In summary, targeting miRNA-182-5p may provide a new strategy for the treatment of asthma.https://www.frontiersin.org/articles/10.3389/fimmu.2022.853848/fullmiR-182-5pNOX4airway inflammationasthmaOvalbumin (OVA) |
| spellingShingle | Zhiguang Wang Zhiguang Wang Yilan Song Yilan Song Jingzhi Jiang Jingzhi Jiang Yihua Piao Yihua Piao Li Li Li Li Qiaoyun Bai Qiaoyun Bai Chang Xu Chang Xu Hanye Liu Hanye Liu Liangchang Li Liangchang Li Hongmei Piao Hongmei Piao Guanghai Yan Guanghai Yan MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4 Frontiers in Immunology miR-182-5p NOX4 airway inflammation asthma Ovalbumin (OVA) |
| title | MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4 |
| title_full | MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4 |
| title_fullStr | MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4 |
| title_full_unstemmed | MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4 |
| title_short | MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4 |
| title_sort | microrna 182 5p attenuates asthmatic airway inflammation by targeting nox4 |
| topic | miR-182-5p NOX4 airway inflammation asthma Ovalbumin (OVA) |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2022.853848/full |
| work_keys_str_mv | AT zhiguangwang microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT zhiguangwang microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT yilansong microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT yilansong microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT jingzhijiang microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT jingzhijiang microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT yihuapiao microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT yihuapiao microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT lili microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT lili microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT qiaoyunbai microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT qiaoyunbai microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT changxu microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT changxu microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT hanyeliu microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT hanyeliu microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT liangchangli microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT liangchangli microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT hongmeipiao microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT hongmeipiao microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT guanghaiyan microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 AT guanghaiyan microrna1825pattenuatesasthmaticairwayinflammationbytargetingnox4 |