Academic Journal
MKP-3 suppresses LPS-induced inflammatory responses in HUVECs via inhibition of p38 MAPK/NF-κB pathway
| العنوان: | MKP-3 suppresses LPS-induced inflammatory responses in HUVECs via inhibition of p38 MAPK/NF-κB pathway |
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| المؤلفون: | Banzragchgarav Unenkhuu, Da Bin Kim, Hong Seok Kim |
| المصدر: | Animal Cells and Systems, Vol 25, Iss 4, Pp 235-244 (2021) |
| بيانات النشر: | Taylor & Francis Group, 2021. |
| سنة النشر: | 2021 |
| المجموعة: | LCC:Medicine (General) LCC:Biology (General) |
| مصطلحات موضوعية: | mkp-3, endothelial cell, inflammation, lipopolysaccharide, endotoxemia, Medicine (General), R5-920, Biology (General), QH301-705.5 |
| الوصف: | Endothelial cell dysfunction and inflammatory responses play critical roles in the development of atherosclerosis. Recent data on the processes underlying atherogenesis indicate the substantial role of endotoxins (lipopolysaccharides; LPS) of the intestinal microflora in the initiation and progression of atherosclerosis. Mitogen-activated protein (MAP) kinase phosphatase-3 (MKP-3) is a cytoplasmic dual-specificity protein phosphatase that specifically binds to and inactivates MAP kinases in mammalian cells, but its biological function in endothelial cell dysfunction and inflammatory responses remains largely unknown. The aim of the present study was to investigate the role of MKP-3 in endotoxin-induced endothelial inflammation by western blotting, quantitative polymerase chain reaction, and immunofluorescence. The results of our study demonstrated that MKP-3 overexpression markedly inhibited the adhesion of human monocytic THP-1 cells to human umbilical vein endothelial cells (HUVECs) by downregulating the expression of vascular cell adhesion protein 1 (VCAM-1) and pro-inflammatory cytokines. In contrast, MKP-3-encoding gene knockdown by small interfering RNA (siRNA) exacerbated LPS-induced endothelial dysfunction. Additionally, we found that MKP-3 overexpression inhibited LPS-induced p38 MAPK phosphorylation and decreased the nuclear translocation of nuclear factor kappa B (NF-κB) after LPS treatment, suggesting its implication in the LPS/Toll-like receptor 4 (TLR4)/p38/NF-κB pathway. Overall, these observations suggest that MKP-3 plays a protective role in endothelial dysfunction and may be a therapeutic target. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1976-8354 2151-2485 19768354 |
| Relation: | https://doaj.org/toc/1976-8354; https://doaj.org/toc/2151-2485 |
| DOI: | 10.1080/19768354.2021.1954551 |
| URL الوصول: | https://doaj.org/article/841f58aa8a2447ecad3e4b3983b17eb3 |
| رقم الانضمام: | edsdoj.841f58aa8a2447ecad3e4b3983b17eb3 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 19768354 21512485 |
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| DOI: | 10.1080/19768354.2021.1954551 |