Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B
Objective To investigate the effects of miR-338-3p on interleukin (IL) -13-induced human bronchial epithelial cell line (BEAS-2B) injury and airway inflammation in mice with ovalbumin (OVA) -induced asthma. Methods OVA was used to replicate an asthma model of mice, which were divided into control gr...
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Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.
2025-03-01
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| Series: | Jichu yixue yu linchuang |
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| Online Access: | https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-3-281-346.pdf |
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| author | FU Haiwei, GUO Weiwei, SHENG Fen, LIU Donghong |
| author_facet | FU Haiwei, GUO Weiwei, SHENG Fen, LIU Donghong |
| author_sort | FU Haiwei, GUO Weiwei, SHENG Fen, LIU Donghong |
| collection | DOAJ |
| description | Objective To investigate the effects of miR-338-3p on interleukin (IL) -13-induced human bronchial epithelial cell line (BEAS-2B) injury and airway inflammation in mice with ovalbumin (OVA) -induced asthma. Methods OVA was used to replicate an asthma model of mice, which were divided into control group, model group, miR-NC agomir and miR-338-3p agomir intervention groups. HE staining microscopy was employed to observe the pathological morphology of lung tissue, while TUNEL staining was used to assess cell apoptosis in lung tissue. ELISA was conducted to measure the levels of interleukin-1β (IL-1β) and tumor necrosis factor (TNF)-α in lung tissue. The BEAS-2B cells were subjected to IL-13-induced injury and divided into control group, IL-13group, IL-13+miR-NC group, and IL-13+miR-338-3p mimic group. Cell viability was assessed with MTT assay. Flow cytometry was employed to evaluate cell apoptosis. The level of IL-1β and TNF-α in cells was measured by ELISA. The targeting relationship between miR-338-3p and Ras homologous (Rho) was investigated using bioinformatics analysis, luciferase assay, Western blot, and functional repair assay. Results Compared to the model group, the miR-338-3p agamid intervention group exhibited a significant reduction in inflammatory cell infiltration and airway wall thickening in lung tissue, as well as decreased cell apoptosis and the level of IL-1β and TNF-α in lung tissue (P＜0.05). Compared to the control group, cell viability of BEAS-2B cells in the IL-13+miR-338-3p mimic group exhibited a significant increase (P＜0.05), while apoptosis and level of IL-1β and TNF-α within the cells demonstrated a notable decrease (P＜0.05). Rho was a target gene of miR-338-3p, and over-expression of Rho attenuated the effect of miR-338-3p mimic on IL-13-induced injury and inflammation in BEAS-2B cells. Conclusions Up-regulation of miR-338-3p can inhibit asthma-related airway inflammation and injury of lung epithelial cells with a potential mechanism targeting at Rho gene. |
| format | Article |
| id | doaj-art-695fca3a52ca40ce90d946546ffc611e |
| institution | DOAJ |
| issn | 1001-6325 |
| language | zho |
| publishDate | 2025-03-01 |
| publisher | Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. |
| record_format | Article |
| series | Jichu yixue yu linchuang |
| spelling | doaj-art-695fca3a52ca40ce90d946546ffc611e2025-08-20T02:53:57ZzhoInstitute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.Jichu yixue yu linchuang1001-63252025-03-0145334635310.16352/j.issn.1001-6325.2025.03.0346Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2BFU Haiwei, GUO Weiwei, SHENG Fen, LIU Donghong0Department of Respiratory Medicine, Taizhou First People′s Hospital, Taizhou 318020, ChinaObjective To investigate the effects of miR-338-3p on interleukin (IL) -13-induced human bronchial epithelial cell line (BEAS-2B) injury and airway inflammation in mice with ovalbumin (OVA) -induced asthma. Methods OVA was used to replicate an asthma model of mice, which were divided into control group, model group, miR-NC agomir and miR-338-3p agomir intervention groups. HE staining microscopy was employed to observe the pathological morphology of lung tissue, while TUNEL staining was used to assess cell apoptosis in lung tissue. ELISA was conducted to measure the levels of interleukin-1β (IL-1β) and tumor necrosis factor (TNF)-α in lung tissue. The BEAS-2B cells were subjected to IL-13-induced injury and divided into control group, IL-13group, IL-13+miR-NC group, and IL-13+miR-338-3p mimic group. Cell viability was assessed with MTT assay. Flow cytometry was employed to evaluate cell apoptosis. The level of IL-1β and TNF-α in cells was measured by ELISA. The targeting relationship between miR-338-3p and Ras homologous (Rho) was investigated using bioinformatics analysis, luciferase assay, Western blot, and functional repair assay. Results Compared to the model group, the miR-338-3p agamid intervention group exhibited a significant reduction in inflammatory cell infiltration and airway wall thickening in lung tissue, as well as decreased cell apoptosis and the level of IL-1β and TNF-α in lung tissue (P＜0.05). Compared to the control group, cell viability of BEAS-2B cells in the IL-13+miR-338-3p mimic group exhibited a significant increase (P＜0.05), while apoptosis and level of IL-1β and TNF-α within the cells demonstrated a notable decrease (P＜0.05). Rho was a target gene of miR-338-3p, and over-expression of Rho attenuated the effect of miR-338-3p mimic on IL-13-induced injury and inflammation in BEAS-2B cells. Conclusions Up-regulation of miR-338-3p can inhibit asthma-related airway inflammation and injury of lung epithelial cells with a potential mechanism targeting at Rho gene.https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-3-281-346.pdfasthma|mir-338-3p|airway inflammation|ras homologous(rho) |
| spellingShingle | FU Haiwei, GUO Weiwei, SHENG Fen, LIU Donghong Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B Jichu yixue yu linchuang asthma|mir-338-3p|airway inflammation|ras homologous(rho) |
| title | Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B |
| title_full | Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B |
| title_fullStr | Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B |
| title_full_unstemmed | Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B |
| title_short | Up-regulation of miR-338-3p alleviatesIL-13-induced injury of human bronchial cell line BEAS-2B |
| title_sort | up regulation of mir 338 3p alleviatesil 13 induced injury of human bronchial cell line beas 2b |
| topic | asthma|mir-338-3p|airway inflammation|ras homologous(rho) |
| url | https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-3-281-346.pdf |
| work_keys_str_mv | AT fuhaiweiguoweiweishengfenliudonghong upregulationofmir3383palleviatesil13inducedinjuryofhumanbronchialcelllinebeas2b |