Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro
In this study, the effects of single immunoglobin IL-1 receptor-related protein (SIGIRR) on tumor necrosis factor- (TNF-) receptor-associated factor 6 (TRAF6) ubiquitination in acute lung injury (ALI) were evaluated in both alveolar epithelial cells and alveolar macrophage cells in vitro. Our result...
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Format: | Article |
Language: | English |
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Wiley
2020-01-01
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Series: | Journal of Immunology Research |
Online Access: | http://dx.doi.org/10.1155/2020/5097920 |
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author | Feng Tian Qiang Lu Jie Lei Yunfeng Ni Nianlin Xie Daixing Zhong Guang Yang Shaokui Si Tao Jiang |
author_facet | Feng Tian Qiang Lu Jie Lei Yunfeng Ni Nianlin Xie Daixing Zhong Guang Yang Shaokui Si Tao Jiang |
author_sort | Feng Tian |
collection | DOAJ |
description | In this study, the effects of single immunoglobin IL-1 receptor-related protein (SIGIRR) on tumor necrosis factor- (TNF-) receptor-associated factor 6 (TRAF6) ubiquitination in acute lung injury (ALI) were evaluated in both alveolar epithelial cells and alveolar macrophage cells in vitro. Our results found that SIGIRR negatively regulated TRAF6 ubiquitination and such SIGIRR inhibition could enhance the TRAF6 expression in both alveolar epithelial cells (AECs) and alveolar macrophage cells (AMCs). SIGIRR knockdown may increase NF-κB activity via TRAF6 regulation by the classical but not the nonclassical NF-κB signaling pathway. Such modulation between TRAF6 and SIGIRR could affect cytokine secretion and exacerbate the immune response; the IL-8, NFKB1, and NFKBIA mRNA levels were reduced after SIGIRR overexpression. The current study reveals the molecular mechanisms of the negative regulatory roles of SIGIRR on the innate immune response related to the LPS/TLR-4 signaling pathway and provides evidence for strategies to clinically treat inflammatory diseases. |
format | Article |
id | doaj-art-4869b58b6fe84636ae81d5dcd442d811 |
institution | Kabale University |
issn | 2314-8861 2314-7156 |
language | English |
publishDate | 2020-01-01 |
publisher | Wiley |
record_format | Article |
series | Journal of Immunology Research |
spelling | doaj-art-4869b58b6fe84636ae81d5dcd442d8112025-02-03T06:05:38ZengWileyJournal of Immunology Research2314-88612314-71562020-01-01202010.1155/2020/50979205097920Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In VitroFeng Tian0Qiang Lu1Jie Lei2Yunfeng Ni3Nianlin Xie4Daixing Zhong5Guang Yang6Shaokui Si7Tao Jiang8Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaDepartment of Respiration, Third Hospital of Baoji, Baoji, ChinaDepartment of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, ChinaIn this study, the effects of single immunoglobin IL-1 receptor-related protein (SIGIRR) on tumor necrosis factor- (TNF-) receptor-associated factor 6 (TRAF6) ubiquitination in acute lung injury (ALI) were evaluated in both alveolar epithelial cells and alveolar macrophage cells in vitro. Our results found that SIGIRR negatively regulated TRAF6 ubiquitination and such SIGIRR inhibition could enhance the TRAF6 expression in both alveolar epithelial cells (AECs) and alveolar macrophage cells (AMCs). SIGIRR knockdown may increase NF-κB activity via TRAF6 regulation by the classical but not the nonclassical NF-κB signaling pathway. Such modulation between TRAF6 and SIGIRR could affect cytokine secretion and exacerbate the immune response; the IL-8, NFKB1, and NFKBIA mRNA levels were reduced after SIGIRR overexpression. The current study reveals the molecular mechanisms of the negative regulatory roles of SIGIRR on the innate immune response related to the LPS/TLR-4 signaling pathway and provides evidence for strategies to clinically treat inflammatory diseases.http://dx.doi.org/10.1155/2020/5097920 |
spellingShingle | Feng Tian Qiang Lu Jie Lei Yunfeng Ni Nianlin Xie Daixing Zhong Guang Yang Shaokui Si Tao Jiang Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro Journal of Immunology Research |
title | Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro |
title_full | Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro |
title_fullStr | Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro |
title_full_unstemmed | Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro |
title_short | Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro |
title_sort | negative effects of sigirr on traf6 ubiquitination in acute lung injury in vitro |
url | http://dx.doi.org/10.1155/2020/5097920 |
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