Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation
Lead (Pb) exposure is widely acknowledged as a risk factor for cardiovascular diseases. Previous studies have established neutrophil involvement in Pb-induced cardiovascular injuries; however, the underlying mechanisms remain unclear. To address this knowledge gap, the binding targets of Pb in neutr...
Saved in:
| Main Authors: | , , , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-01-01
|
| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324016749 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1823856918154706944 |
|---|---|
| author | Qiying Nong Yanjun Wu Suhui Liu Yinyin Tang Jiayun Wu Hongmei Huang Jiaying Hong Yiru Qin Ruimei Xu Wenxia Zhao Baowei Chen Zhenlie Huang Ligang Hu Na Zhao Yongshun Huang |
| author_facet | Qiying Nong Yanjun Wu Suhui Liu Yinyin Tang Jiayun Wu Hongmei Huang Jiaying Hong Yiru Qin Ruimei Xu Wenxia Zhao Baowei Chen Zhenlie Huang Ligang Hu Na Zhao Yongshun Huang |
| author_sort | Qiying Nong |
| collection | DOAJ |
| description | Lead (Pb) exposure is widely acknowledged as a risk factor for cardiovascular diseases. Previous studies have established neutrophil involvement in Pb-induced cardiovascular injuries; however, the underlying mechanisms remain unclear. To address this knowledge gap, the binding targets of Pb in neutrophils and their roles in regulating neutrophil extracellular trap (NET) formation were investigated. Furthermore, their impact on Pb-induced vascular inflammation and other cardiovascular injuries was studied in mice. Our findings indicate, for the first time, that Pb binds to β-actin in neutrophils, influencing NET formation. Inhibition of actin polymerization reduces the release of extracellular myeloperoxidase, neutrophil elastase, and citrullinated histone H3, indicating an impediment in NET formation. Furthermore, Pb exposure exacerbates blood pressure and vascular inflammation in vascular tissues, leading to abnormal aortic blood flow in mice. These injuries are potentially associated with NET formation, which is supported by the positive correlation between NETs and vascular inflammation. Importantly, the inhibition of actin polymerization mitigates Pb-induced vascular inflammation and regulates systolic blood pressure by reducing NET formation. Collectively, our findings provide novel insights into the mechanism underlying Pb-induced cardiovascular injury, contributing to the management of the escalating risk associated with Pb-induced cardiovascular damage. |
| format | Article |
| id | doaj-art-8f39bf7e27c443829f3a511386021b0c |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-8f39bf7e27c443829f3a511386021b0c2025-02-12T05:29:56ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01290117598Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammationQiying Nong0Yanjun Wu1Suhui Liu2Yinyin Tang3Jiayun Wu4Hongmei Huang5Jiaying Hong6Yiru Qin7Ruimei Xu8Wenxia Zhao9Baowei Chen10Zhenlie Huang11Ligang Hu12Na Zhao13Yongshun Huang14Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; Guangming District Center for Disease Control and Prevention, Shenzhen 518016, China; Department of Toxicology, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; School of Public Health, Sun Yat-sen University, Guangzhou 510080, ChinaState Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; School of Public Health, Sun Yat-sen University, Guangzhou 510080, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, ChinaMaterial Microanalysis Division, Instrumental Analysis & Research Center, Sun Yat-Sen University, Guangzhou 510275, ChinaMaterial Microanalysis Division, Instrumental Analysis & Research Center, Sun Yat-Sen University, Guangzhou 510275, ChinaGuangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, School of Marine Sciences, Sun Yat-Sen University, Guangzhou 510275, ChinaDepartment of Toxicology, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaState Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; Institute of Environment and Health, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310000, ChinaGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; Corresponding author at: Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China.Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; Department of Toxicology, School of Public Health, Southern Medical University, Guangzhou 510515, China; School of Public Health, Sun Yat-sen University, Guangzhou 510080, China; School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China; Corresponding author at: Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China.Lead (Pb) exposure is widely acknowledged as a risk factor for cardiovascular diseases. Previous studies have established neutrophil involvement in Pb-induced cardiovascular injuries; however, the underlying mechanisms remain unclear. To address this knowledge gap, the binding targets of Pb in neutrophils and their roles in regulating neutrophil extracellular trap (NET) formation were investigated. Furthermore, their impact on Pb-induced vascular inflammation and other cardiovascular injuries was studied in mice. Our findings indicate, for the first time, that Pb binds to β-actin in neutrophils, influencing NET formation. Inhibition of actin polymerization reduces the release of extracellular myeloperoxidase, neutrophil elastase, and citrullinated histone H3, indicating an impediment in NET formation. Furthermore, Pb exposure exacerbates blood pressure and vascular inflammation in vascular tissues, leading to abnormal aortic blood flow in mice. These injuries are potentially associated with NET formation, which is supported by the positive correlation between NETs and vascular inflammation. Importantly, the inhibition of actin polymerization mitigates Pb-induced vascular inflammation and regulates systolic blood pressure by reducing NET formation. Collectively, our findings provide novel insights into the mechanism underlying Pb-induced cardiovascular injury, contributing to the management of the escalating risk associated with Pb-induced cardiovascular damage.http://www.sciencedirect.com/science/article/pii/S0147651324016749Heavy metalActin polymerizationNeutrophil extracellular trapCardiovascular injuryHypertension |
| spellingShingle | Qiying Nong Yanjun Wu Suhui Liu Yinyin Tang Jiayun Wu Hongmei Huang Jiaying Hong Yiru Qin Ruimei Xu Wenxia Zhao Baowei Chen Zhenlie Huang Ligang Hu Na Zhao Yongshun Huang Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation Ecotoxicology and Environmental Safety Heavy metal Actin polymerization Neutrophil extracellular trap Cardiovascular injury Hypertension |
| title | Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation |
| title_full | Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation |
| title_fullStr | Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation |
| title_full_unstemmed | Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation |
| title_short | Lead-induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation |
| title_sort | lead induced actin polymerization aggravates neutrophil extracellular trap formation and contributes to vascular inflammation |
| topic | Heavy metal Actin polymerization Neutrophil extracellular trap Cardiovascular injury Hypertension |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324016749 |
| work_keys_str_mv | AT qiyingnong leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT yanjunwu leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT suhuiliu leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT yinyintang leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT jiayunwu leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT hongmeihuang leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT jiayinghong leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT yiruqin leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT ruimeixu leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT wenxiazhao leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT baoweichen leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT zhenliehuang leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT liganghu leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT nazhao leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation AT yongshunhuang leadinducedactinpolymerizationaggravatesneutrophilextracellulartrapformationandcontributestovascularinflammation |