LPS enhances TLR4 expression and IFNγ production via the TLR4/IRAK/NFκB signaling pathway in rat pulmonary arterial smooth muscle cells.
Mol Med Rep
; 16(3): 3111-3116, 2017 Sep.
Article
en En
| MEDLINE
| ID: mdl-28714001
ABSTRACT
The aim of the present study was to investigate the role of the Tolllike receptor (TLR)4 signaling pathway in cellular response to lipopolysaccharide (LPS) in rat pulmonary artery smooth muscle cells (PASMCs). Chronic obstructive pulmonary disease (COPD) rats were established with passive inhaling cigarette smoke plus injection of LPS. The TLR4 protein in lung tissues was determined with immunohistochemical staining and protein levels of the components of the TLR4 pathway in PASMCs were analyzed with western blotting. The production of interferon (IFN)γ upon LPS stimulation in PASMCs was measured with ELISA. TLR4 expression in lung tissue from COPD rats was increased obviously compared with that in normal group. LPS enhances TLR4 expression in rat PASMCs and induced production of IFNγ dramatically. LPS treatment resulted in increased phosphorinterleukin1 receptorassociated kinase (IRAK), IκB and IκB kinase, as well as the total protein of nuclear factor (NF)κB p65. TLR4 inhibitor TAK242, IRAK1/4 inhibitor and NFκB inhibitor Bay 117082 were capable of suppressing the effects of LPS. TLR4 signaling pathway is functional in PASMCs, and may be involved in the inflammatory response during the pathogenesis of COPD.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Arteria Pulmonar
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Lipopolisacáridos
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FN-kappa B
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Interferón gamma
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Miocitos del Músculo Liso
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Receptor Toll-Like 4
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Quinasas Asociadas a Receptores de Interleucina-1
Límite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Año:
2017
Tipo del documento:
Article