American Journal of Translational Research | |
NF-κB protects human neuroblastoma cells from nitric oxide-induced apoptosis through upregulating biglycan | |
Lei Wang1  | |
关键词: Nuclear factor-kappaB; neuroblastoma; nitric oxide; apoptosis; biglycan; | |
DOI : | |
学科分类:医学(综合) | |
来源: e-Century Publishing Corporation | |
【 摘 要 】
Excessive nitric oxide (NO) produced in inflammation may result in oxidative stress, which is closely related to the neurodegenerative diseases and brain damage. Massive NO production can enhance NF-κB activity in various neural cells, but the function of this activation by NO and the target genes transactivated by NF-κB are still largely unknown. In the present study, our results showed sodium nitropruside (SNP), a NO donor, triggered apoptotic cell death and NF-κB activation in human neuroblastoma SH-EP1 cells, and inhibition of NF-κB activation by its super endogenous inhibitor, I-κBαM, sensitized SH-EP1 cells to NO-induced apoptosis. Conversely, NF-κB activation induced by insulin-like growth factor (IGF)-1 antagonizes NO-induced apoptotic cell death in SH-EP1 cells. In addition, cDNA microarray analysis showed biglycan, an extracellular glycoprotein, was up-regulated by NF-κB, and recombinant biglycan protein conferred a protective effect on NF-κB mediated NO-induced apoptotic cell death in SH-EP1 cells. These findings suggest biglycan may serve as a potential target in preventing NO-induced neurodegenerative diseases.
【 授权许可】
CC BY-NC
【 预 览 】
Files | Size | Format | View |
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RO201901231948578ZK.pdf | 905KB | download |