Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB
Autor(a) principal: | |
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Data de Publicação: | 2024 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Clinics |
Texto Completo: | https://revistas.usp.br/clinics/article/view/237028 |
Resumo: | Objectives: The pathogenic mechanisms of Thromboangiitis Obliterans (TAO) are not entirely known and autoimmune inflammation plays a vital role in the initiation and continuance of TAO activity. The authors investigated in this study the role of the TLR signaling pathway in the pathogenesis of TAO. Methods: First, the authors detected the expressions of MyD88, TRIF and NF-κB in vascular walls of 46 patients with TAO and 32 patients with trauma and osteosarcoma by western blot assay. Second, the authors detected the cellular localization of MyD88, TRIF and NF-κB in vascular walls of patients with TAO by immunofluorescent assay. Results: The protein expressions of MyD88, TRIF and NF-κB were much higher in vascular walls of TAO patients (p < 0.05). Higher expressions of MyD88 and NF-κB were detected both on vascular endothelial and vascular smooth muscle cells of TAO patients. However, higher expression of TRIF was just detected on vascular smooth muscle cells of TAO patients. Conclusions: These dates suggest that the TLR signaling pathway might play an important role in the pathogenesis of TAO, it might induce vasospasm, vasculitis and thrombogenesis to lead to the pathogenesis and progression of TAO. |
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Clinics |
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Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κBThromboangiitis obliteransTLR signaling pathwayMyD88TRIFNF-κBPathogenic mechanismObjectives: The pathogenic mechanisms of Thromboangiitis Obliterans (TAO) are not entirely known and autoimmune inflammation plays a vital role in the initiation and continuance of TAO activity. The authors investigated in this study the role of the TLR signaling pathway in the pathogenesis of TAO. Methods: First, the authors detected the expressions of MyD88, TRIF and NF-κB in vascular walls of 46 patients with TAO and 32 patients with trauma and osteosarcoma by western blot assay. Second, the authors detected the cellular localization of MyD88, TRIF and NF-κB in vascular walls of patients with TAO by immunofluorescent assay. Results: The protein expressions of MyD88, TRIF and NF-κB were much higher in vascular walls of TAO patients (p < 0.05). Higher expressions of MyD88 and NF-κB were detected both on vascular endothelial and vascular smooth muscle cells of TAO patients. However, higher expression of TRIF was just detected on vascular smooth muscle cells of TAO patients. Conclusions: These dates suggest that the TLR signaling pathway might play an important role in the pathogenesis of TAO, it might induce vasospasm, vasculitis and thrombogenesis to lead to the pathogenesis and progression of TAO.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2024-02-15info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://revistas.usp.br/clinics/article/view/23702810.1016/Clinics; Vol. 79 (2024); 100357Clinics; v. 79 (2024); 100357Clinics; Vol. 79 (2024); 1003571980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://revistas.usp.br/clinics/article/view/237028/214021Copyright (c) 2024 Clinicsinfo:eu-repo/semantics/openAccessGuo, FacaiBi, YanYin, JiangyanGuo, Yi2025-06-17T18:45:43Zoai:revistas.usp.br:article/237028Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2025-06-17T18:45:43Clinics - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
title |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
spellingShingle |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB Guo, Facai Thromboangiitis obliterans TLR signaling pathway MyD88 TRIF NF-κB Pathogenic mechanism |
title_short |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
title_full |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
title_fullStr |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
title_full_unstemmed |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
title_sort |
Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB |
author |
Guo, Facai |
author_facet |
Guo, Facai Bi, Yan Yin, Jiangyan Guo, Yi |
author_role |
author |
author2 |
Bi, Yan Yin, Jiangyan Guo, Yi |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Guo, Facai Bi, Yan Yin, Jiangyan Guo, Yi |
dc.subject.por.fl_str_mv |
Thromboangiitis obliterans TLR signaling pathway MyD88 TRIF NF-κB Pathogenic mechanism |
topic |
Thromboangiitis obliterans TLR signaling pathway MyD88 TRIF NF-κB Pathogenic mechanism |
description |
Objectives: The pathogenic mechanisms of Thromboangiitis Obliterans (TAO) are not entirely known and autoimmune inflammation plays a vital role in the initiation and continuance of TAO activity. The authors investigated in this study the role of the TLR signaling pathway in the pathogenesis of TAO. Methods: First, the authors detected the expressions of MyD88, TRIF and NF-κB in vascular walls of 46 patients with TAO and 32 patients with trauma and osteosarcoma by western blot assay. Second, the authors detected the cellular localization of MyD88, TRIF and NF-κB in vascular walls of patients with TAO by immunofluorescent assay. Results: The protein expressions of MyD88, TRIF and NF-κB were much higher in vascular walls of TAO patients (p < 0.05). Higher expressions of MyD88 and NF-κB were detected both on vascular endothelial and vascular smooth muscle cells of TAO patients. However, higher expression of TRIF was just detected on vascular smooth muscle cells of TAO patients. Conclusions: These dates suggest that the TLR signaling pathway might play an important role in the pathogenesis of TAO, it might induce vasospasm, vasculitis and thrombogenesis to lead to the pathogenesis and progression of TAO. |
publishDate |
2024 |
dc.date.none.fl_str_mv |
2024-02-15 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://revistas.usp.br/clinics/article/view/237028 10.1016/ |
url |
https://revistas.usp.br/clinics/article/view/237028 |
identifier_str_mv |
10.1016/ |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://revistas.usp.br/clinics/article/view/237028/214021 |
dc.rights.driver.fl_str_mv |
Copyright (c) 2024 Clinics info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Copyright (c) 2024 Clinics |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
dc.source.none.fl_str_mv |
Clinics; Vol. 79 (2024); 100357 Clinics; v. 79 (2024); 100357 Clinics; Vol. 79 (2024); 100357 1980-5322 1807-5932 reponame:Clinics instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Clinics |
collection |
Clinics |
repository.name.fl_str_mv |
Clinics - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
||clinics@hc.fm.usp.br |
_version_ |
1839536619220107264 |