PM2.5 increases mouse blood pressure by activating toll-like receptor 3
Background and aims: Plenty of literature has documented that fine particulate matter (PM2.5) exposure is related to blood pressure (BP) elevation. Vascular dysfunction is the initiation of cardiovascular diseases, such as hypertension. This thesis set out to assess the role of Toll-like receptor 3...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2022-04-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651322002081 |
| _version_ | 1818284185789399040 |
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| author | Jinna Zhang Rucheng Chen Guoqing Zhang Yixuan Wang Jing Peng Renjie Hu Ran Li Weijia Gu Lu Zhang Qinghua Sun Cuiqing Liu |
| author_facet | Jinna Zhang Rucheng Chen Guoqing Zhang Yixuan Wang Jing Peng Renjie Hu Ran Li Weijia Gu Lu Zhang Qinghua Sun Cuiqing Liu |
| author_sort | Jinna Zhang |
| collection | DOAJ |
| description | Background and aims: Plenty of literature has documented that fine particulate matter (PM2.5) exposure is related to blood pressure (BP) elevation. Vascular dysfunction is the initiation of cardiovascular diseases, such as hypertension. This thesis set out to assess the role of Toll-like receptor 3 (TLR3) in the increase in BP induced by PM2.5. Methods: C57BL/6 and TLR3 deficient (TLR3-/-) male mice were randomly allocated to filtered air chamber or real-world inhaled concentrated PM2.5 chamber. BP was evaluated using non-invasive BP recordings. After euthanasia, the aortas and small mesenteric arteries (SMAs) were isolated, and vascular tone was measured using a wire myograph. Leucocytes were detached to assess myeloid-derived suppressor cells using flow cytometry. siRNA transfection was performed to silence TLR3 expression in the human vascular endothelial cells incubated with PM2.5. The gene expression levels of inflammation, adhesion molecules, and oxidative stress in the aortas were assessed by quantitative PCR. Results: Exposure to PM2.5 increased mouse BP, and TLR3 deficiency protected against PM2.5 exposure-induced BP increase. Additionally, the injury of vascular function in the aortas and SMAs was inhibited in TLR3-/- mice. The intercellular adhesion molecule-1 (ICAM-1) was attenuated in TLR3-/- mice, accompanied by the inhibition of inflammatory and oxidized genes of the aortas, such as F4/80, interleukin-6, interleukin-1 beta, and NADPH oxidase 4. In vitro, the enhanced mRNA expression of genes encoding inflammation, oxidative stress, and ICAM-1 by PM2.5 was inhibited by TLR3 silence as well. Conclusions: PM2.5 exposure increased BP via TLR3 activation and impaired vascular function. |
| first_indexed | 2024-12-13T00:48:47Z |
| format | Article |
| id | doaj.art-510e8012db9c486cb75e67f9f3bc5a73 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-12-13T00:48:47Z |
| publishDate | 2022-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-510e8012db9c486cb75e67f9f3bc5a732022-12-22T00:04:58ZengElsevierEcotoxicology and Environmental Safety0147-65132022-04-01234113368PM2.5 increases mouse blood pressure by activating toll-like receptor 3Jinna Zhang0Rucheng Chen1Guoqing Zhang2Yixuan Wang3Jing Peng4Renjie Hu5Ran Li6Weijia Gu7Lu Zhang8Qinghua Sun9Cuiqing Liu10School of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaSchool of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaCorrespondence to: School of Public Health, Zhejiang Chinese Medical University, 548 Binwen Rd Hangzhou, 310053 China.; School of Public Health, International Science and Technology Cooperation Base of Air Pollution and Health, Zhejiang Chinese Medical University, Hangzhou, ChinaBackground and aims: Plenty of literature has documented that fine particulate matter (PM2.5) exposure is related to blood pressure (BP) elevation. Vascular dysfunction is the initiation of cardiovascular diseases, such as hypertension. This thesis set out to assess the role of Toll-like receptor 3 (TLR3) in the increase in BP induced by PM2.5. Methods: C57BL/6 and TLR3 deficient (TLR3-/-) male mice were randomly allocated to filtered air chamber or real-world inhaled concentrated PM2.5 chamber. BP was evaluated using non-invasive BP recordings. After euthanasia, the aortas and small mesenteric arteries (SMAs) were isolated, and vascular tone was measured using a wire myograph. Leucocytes were detached to assess myeloid-derived suppressor cells using flow cytometry. siRNA transfection was performed to silence TLR3 expression in the human vascular endothelial cells incubated with PM2.5. The gene expression levels of inflammation, adhesion molecules, and oxidative stress in the aortas were assessed by quantitative PCR. Results: Exposure to PM2.5 increased mouse BP, and TLR3 deficiency protected against PM2.5 exposure-induced BP increase. Additionally, the injury of vascular function in the aortas and SMAs was inhibited in TLR3-/- mice. The intercellular adhesion molecule-1 (ICAM-1) was attenuated in TLR3-/- mice, accompanied by the inhibition of inflammatory and oxidized genes of the aortas, such as F4/80, interleukin-6, interleukin-1 beta, and NADPH oxidase 4. In vitro, the enhanced mRNA expression of genes encoding inflammation, oxidative stress, and ICAM-1 by PM2.5 was inhibited by TLR3 silence as well. Conclusions: PM2.5 exposure increased BP via TLR3 activation and impaired vascular function.http://www.sciencedirect.com/science/article/pii/S0147651322002081Fine particulate matterTLR3Blood pressureVascular functionInflammation |
| spellingShingle | Jinna Zhang Rucheng Chen Guoqing Zhang Yixuan Wang Jing Peng Renjie Hu Ran Li Weijia Gu Lu Zhang Qinghua Sun Cuiqing Liu PM2.5 increases mouse blood pressure by activating toll-like receptor 3 Ecotoxicology and Environmental Safety Fine particulate matter TLR3 Blood pressure Vascular function Inflammation |
| title | PM2.5 increases mouse blood pressure by activating toll-like receptor 3 |
| title_full | PM2.5 increases mouse blood pressure by activating toll-like receptor 3 |
| title_fullStr | PM2.5 increases mouse blood pressure by activating toll-like receptor 3 |
| title_full_unstemmed | PM2.5 increases mouse blood pressure by activating toll-like receptor 3 |
| title_short | PM2.5 increases mouse blood pressure by activating toll-like receptor 3 |
| title_sort | pm2 5 increases mouse blood pressure by activating toll like receptor 3 |
| topic | Fine particulate matter TLR3 Blood pressure Vascular function Inflammation |
| url | http://www.sciencedirect.com/science/article/pii/S0147651322002081 |
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