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Text
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URL Address
<a href="http://doi.org/10.5551/jat.29421" target="_blank" rel="noreferrer noopener">http://doi.org/10.5551/jat.29421</a>
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Pages
1317-1337
Issue
12
Volume
22
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Title
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Interleukin-1 Receptor-Associated Kinase 1/4 as a Novel Target for Inhibiting Neointimal Formation After Carotid Balloon Injury
Publisher
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Journal of Atherosclerosis and Thrombosis
Date
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2015
2015
Subject
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Cardiovascular System & Cardiology; in-vivo; smooth-muscle-cells; signaling pathways; hyperplasia; NF kappa B; arterial injury; bacterial infections; Carotid artery balloon injury; intimal; irak-4 protein; IRAK1/4; muscle cell; Neointimal formation; NF kappa B; TLR4; toll-like-receptor; toll-like-receptor-4 expression; Vascular smooth
Creator
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Bai S R; Li D Y; Zhou Z M; Cao J L; Xu T D; Zhang X T; Wang Y; Guo J S; Zhang Y B
Description
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Aim: Interleukin-1 receptor-associated kinase 1 (IRAK1) and IRAK4 play essential roles in the induction of inflammatory gene products. We aimed to investigate the effect of the inhibition of IRAK1 and IRAK4 kinase activities on neointimal formation in rats with carotid artery balloon injuries using the IRAK1/4 inhibitor N-(2-Morpholinylethyl)-2-(3-nitrobenzoylamido)-benzimidazole, a cell-permeable benzimidazole compound. Methods: Wistar rats and vascular smooth muscle cells (VSMCs) isolated from the thoracic aortas were used. Toll-like receptor 4 (TLR4)-mediated nuclear factor kappa B (NF kappa B) signaling pathway was revealed by microarrays analysis. In addition, the differential expression of the TLR4 pathway genes, including TLR4, IRAK1, I kappa B alpha, and interleukin-1 beta (IL-1 beta), was confirmed by quantitative real-time polymerase chain reaction. Immunohistochemical staining, elastic-van Gieson and Masson staining, 5-ethynyl-2'-deoxyuridine staining, enzyme-linked immunosorbent assay, transwell migration assay and western blotting were also contributed for relevant detection. Results: The expression of TLR4 protein gradually increased at days 1, 3, 7, and 21 after balloon injury compared with the uninjured group. The dual inhibition of IRAK1 and IRAK4 attenuated neointimal formation and fibrotic remodeling after injury in vivo and suppressed VSMC proliferation and migration in vitro. The production of mediators such as tumor necrosis factor-alpha and IL-1 beta in injured arteries were also reduced by the inhibition of IRAK1 and IRAK4. The expression of NF kappa B p65- and F4/80-positive cells in inhibitor rats were fewer than those in control rats at day 7, while IRAK1 expression was markedly higher at day 3 in inhibitor rats. Furthermore, western blotting analysis revealed that the IRAK1/4 inhibitor suppressed the IRAK1 and IRAK4 kinase activities and the activation of the TLR4-mediated NF kappa B pathway in vivo and in vitro. Conclusions: This study suggested that IRAK1/4 could serve as a potential therapeutic target to suppress neointimal formation in carotid arteries after balloon injury through the TLR4/NF kappa B signaling pathway.
Identifier
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<a href="http://doi.org/10.5551/jat.29421" target="_blank" rel="noreferrer noopener">10.5551/jat.29421</a>
Format
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Journal Article or Conference Abstract Publication
2015
arterial injury
Bacterial Infections
Bai S R
Cao J L
Cardiovascular System & Cardiology
Carotid artery balloon injury
Guo J S
Hyperplasia
in-vivo
intimal
irak-4 protein
IRAK1/4
Journal Article or Conference Abstract Publication
Journal of Atherosclerosis and Thrombosis
Li D Y
muscle cell
Neointimal formation
NF kappa B
signaling pathways
smooth-muscle-cells
TLR4
toll-like-receptor
toll-like-receptor-4 expression
Vascular smooth
Wang Y
Xu T D
Zhang X T
Zhang Y B
Zhou Z M