Knockdown of low density lipoprotein receptor-related protein 1 in chondrocytes / 中国组织工程研究
Chinese Journal of Tissue Engineering Research
;
(53): 2171-2177, 2016.
Artículo
en Chino
| WPRIM
| ID: wpr-486184
ABSTRACT
BACKGROUND:
Tumor necrosis factor α, as a pathogenic factor, induces the inflammatory reaction mainlyvia the activation of the nuclear factor kappa B signaling pathway. Low density lipoprotein receptor-related protein 1 (LRP1) is involved in the regulation of the inflammatory reaction induced by cytokines.OBJECTIVE:
To study the effect of knockdown of LRP1 on tumor necrosis factor α-induced inflammatory reaction.METHODS:
Primary cultured rat chondrocytes were transfected with lentivirus-mediated RNA interference to knockdown LRP1 gene. Three days after lentivirus transfection, chondrocytes were pretreated with Bay 11-7082 (10 μmol/L) for 30 minutes prior to the addition of tumor necrosis factor α (30 μg/L) for 30 minutes. Signaling protein and mRNA expressions in chondrocytes were detected by western blot assay and real-time PCR analysis, respectively. Chondrocytes were pretreated with or not Bay 11-7082 (10 μmol/L) 30 minutes prior to the addition of tumor necrosis factor α (30 μg/L) for 12 hours after starvation in DMEM for overnight, and the culture medium was colected for ELISA determination of matrix metaloproteinase 13 level. RESULTS ANDCONCLUSION:
Tumor necrosis factor α receptor 1 expression was upregulated in chondrocytes after lentivirus-induced knockdown of LRP1. Increased expression of inducible nitric oxide synthase and activation of the nuclear factor kappa B signaling pathway were found after the addition of tumor necrosis factor α in shLRP1 group. Moreover, increased level of matrix metaloproteinase 13 was determined by ELISA. Taken together, knockdown of LRP1 up-regulates the expression of tumor necrosis factor α-induced inducible nitric oxide synthase and matrix metaloproteinase 13 through the activation of the nuclear factor kappa B signaling pathway.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Chinese Journal of Tissue Engineering Research
Año:
2016
Tipo del documento:
Artículo
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