HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication
More and more clinical evidence shows that occupational medicamentose-like dermatitis due to trichloroethylene (OMDT) patients often present immune kidney damage. However, the exact mechanisms of cell-to-cell transmission in TCE-induced immune kidney damage remain poorly understood. The present stud...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-07-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323005468 |
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| author | Xuesong Zhang Haibo Xie Zhibing Liu Jiaxiang Zhang Lihua Deng Qifeng Wu Yuansheng Duan Feng Wang Changhao Wu Qixing Zhu |
| author_facet | Xuesong Zhang Haibo Xie Zhibing Liu Jiaxiang Zhang Lihua Deng Qifeng Wu Yuansheng Duan Feng Wang Changhao Wu Qixing Zhu |
| author_sort | Xuesong Zhang |
| collection | DOAJ |
| description | More and more clinical evidence shows that occupational medicamentose-like dermatitis due to trichloroethylene (OMDT) patients often present immune kidney damage. However, the exact mechanisms of cell-to-cell transmission in TCE-induced immune kidney damage remain poorly understood. The present study aimed to explore the role of high mobility group box-1 (HMGB 1) in glomerular endothelial cell-podocyte transmission. 17 OMDT patients and 34 controls were enrolled in this study. We observed that OMDT patients had renal function injury, endothelial cell activation and podocyte injury, and these indicators were associated with serum HMGB 1. To gain mechanistic insight, a TCE-sensitized BALB/c mouse model was established under the interventions of sirtuin 1 (SIRT 1) activator SRT 1720 (0.1 ml, 5 mg/kg) and receptor for advanced glycation end products (RAGE) inhibitor FPS-ZM 1 (0.1 ml, 1.5 mg/kg). We identified HMGB 1 acetylation and its endothelial cytoplasmic translocation following TCE sensitization, but SRT 1720 abolished the process. RAGE was located on podocytes and co-precipitated with extracellular acetylated HMGB 1, promoting podocyte injury, while SRT 1720 and FPS-ZM 1 both alleviated podocyte injury. The results demonstrate that interventions to upstream and downstream pathways of HMGB 1 may weaken glomerular endothelial cell-podocyte transmission, thereby alleviating TCE-induced immune renal injury. |
| first_indexed | 2024-03-13T07:44:02Z |
| format | Article |
| id | doaj.art-aa0ade7773184208b8194e56679e1fe8 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-03-13T07:44:02Z |
| publishDate | 2023-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-aa0ade7773184208b8194e56679e1fe82023-06-03T04:21:33ZengElsevierEcotoxicology and Environmental Safety0147-65132023-07-01259115042HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communicationXuesong Zhang0Haibo Xie1Zhibing Liu2Jiaxiang Zhang3Lihua Deng4Qifeng Wu5Yuansheng Duan6Feng Wang7Changhao Wu8Qixing Zhu9Department of Occupational Health and Environmental Health, School of Public Health, Anhui Medical University, Hefei, Anhui, China; Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, ChinaDepartment of Nephropathy, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, ChinaKey Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, China; Department of Dermatology, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, ChinaDepartment of Occupational Health and Environmental Health, School of Public Health, Anhui Medical University, Hefei, Anhui, China; Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, ChinaShenzhen Prevention and Treatment Center for Occupational Disease, Shenzhen, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, Guangdong, ChinaDepartment of Occupational Health and Environmental Health, School of Public Health, Anhui Medical University, Hefei, Anhui, China; Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, ChinaDepartment of Dermatology, Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, ChinaFaculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom; Corresponding author.Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, China; Department of Dermatology, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China; Corresponding author at: Department of Dermatology, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.More and more clinical evidence shows that occupational medicamentose-like dermatitis due to trichloroethylene (OMDT) patients often present immune kidney damage. However, the exact mechanisms of cell-to-cell transmission in TCE-induced immune kidney damage remain poorly understood. The present study aimed to explore the role of high mobility group box-1 (HMGB 1) in glomerular endothelial cell-podocyte transmission. 17 OMDT patients and 34 controls were enrolled in this study. We observed that OMDT patients had renal function injury, endothelial cell activation and podocyte injury, and these indicators were associated with serum HMGB 1. To gain mechanistic insight, a TCE-sensitized BALB/c mouse model was established under the interventions of sirtuin 1 (SIRT 1) activator SRT 1720 (0.1 ml, 5 mg/kg) and receptor for advanced glycation end products (RAGE) inhibitor FPS-ZM 1 (0.1 ml, 1.5 mg/kg). We identified HMGB 1 acetylation and its endothelial cytoplasmic translocation following TCE sensitization, but SRT 1720 abolished the process. RAGE was located on podocytes and co-precipitated with extracellular acetylated HMGB 1, promoting podocyte injury, while SRT 1720 and FPS-ZM 1 both alleviated podocyte injury. The results demonstrate that interventions to upstream and downstream pathways of HMGB 1 may weaken glomerular endothelial cell-podocyte transmission, thereby alleviating TCE-induced immune renal injury.http://www.sciencedirect.com/science/article/pii/S0147651323005468TrichloroethyleneEndothelial cell-podocyte transmissionHMGB 1Acetylation·SIRT 1RAGE |
| spellingShingle | Xuesong Zhang Haibo Xie Zhibing Liu Jiaxiang Zhang Lihua Deng Qifeng Wu Yuansheng Duan Feng Wang Changhao Wu Qixing Zhu HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication Ecotoxicology and Environmental Safety Trichloroethylene Endothelial cell-podocyte transmission HMGB 1 Acetylation ·SIRT 1 RAGE |
| title | HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication |
| title_full | HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication |
| title_fullStr | HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication |
| title_full_unstemmed | HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication |
| title_short | HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication |
| title_sort | hmgb 1 acetylation mediates trichloroethylene induced immune kidney injury by facilitating endothelial cell podocyte communication |
| topic | Trichloroethylene Endothelial cell-podocyte transmission HMGB 1 Acetylation ·SIRT 1 RAGE |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323005468 |
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