Reactive oxygen species (ROS)-responsive nanomedicine for RNAi-based cancer therapy

Nanoscale ◽  
2018 ◽  
Vol 10 (1) ◽  
pp. 203-214 ◽  
Author(s):  
Yang Li ◽  
Hongzhen Bai ◽  
Hebin Wang ◽  
Youqing Shen ◽  
Guping Tang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Sirna Delivery ◽  
Reactive Oxygen ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Tumor Site ◽  
Delivery Vehicle ◽  
Endothelial Growth Factor

A reactive oxygen species (ROS)-responsive boronic vehicle with an exterior lipid envelope was developed for systemic vascular endothelial growth factor (VEGF) siRNA delivery. This unique architecture of the delivery vehicle offers enhanced siRNA delivery capability and timely siRNA release at the tumor site.

Reactive Oxygen Species Regulate Angiogenesis and Tumor Growth through Vascular Endothelial Growth Factor

2007 ◽  
Vol 67 (22) ◽  
pp. 10823-10830 ◽  
Author(s):  
Chang Xia ◽  
Qiao Meng ◽  
Ling-Zhi Liu ◽  
Yongyut Rojanasakul ◽  
Xin-Ru Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Growth ◽  
Reactive Oxygen ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Endothelial Growth Factor

scholarly journals Retinoic Acid Is a Cofactor for Translational Regulation of Vascular Endothelial Growth Factor in Human Endometrial Stromal Cells

2010 ◽  
Vol 24 (1) ◽  
pp. 148-160 ◽  
Author(s):  
Neil Sidell ◽  
Yue Feng ◽  
Lijuan Hao ◽  
Juanjuan Wu ◽  
Jie Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Endothelial Growth Factor ◽  
Retinoic Acid ◽  
Growth Factor ◽  
Stromal Cells ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Transcriptional Activators ◽  
Endometrial Stromal Cells ◽  
Endothelial Growth Factor

Abstract Vascular endothelial growth factor (VEGF) and endometrial angiogenesis play a critical role in successful embryonic implantation. Despite many studies of the effects of estrogen and progesterone on VEGF expression, its focal regulation at the site of implantation is unknown. Retinoic acid (RA) has been reported to regulate VEGF in a variety of cell types. Because localized RA synthesis occurs within the periimplantation endometrium, we tested the possibility that RA regulates VEGF production in endometrial stromal cells. Using primary and telomerase-immortalized human endometrial stromal cells, we determined that RA alone did not alter constitutive levels of VEGF production, but markedly amplified secretion when the cells were cotreated with activators of VEGF gene transcription (12-O-tetradecanoyl phorbol-13-acetate, TPA; TGF-β; and IL-1β). Whereas TPA or TGF-β alone stimulated VEGF promoter activity and up-regulated mRNA levels, significant protein secretion was detected only after RA was added to the culture systems. Analysis of retinoids in secretory phase endometrial biopsies indicated that endogenous RA accumulated at concentrations sufficient to induce VEGF secretion. Polyribosome profile analysis showed that the addition of RA to transcriptional activators of VEGF shifted the translational suppressed VEGF mRNA transcripts into larger polyribosome complexes engaged in active translation. Although the precise mechanism(s) of the RA effect remains to be defined, it appears to be mediated by reactive oxygen species; the antioxidant N-acetylcysteine inhibited RA+TPA-stimulated secretion of VEGF by more than 80%. Together, our results demonstrate that in human endometrial stromal cells, RA can combine with transcriptional activators of VEGF to augment VEGF secretion through a translational mechanism of action mediated by reactive oxygen species. These findings suggest a link between the spatiotemporal changes of retinoid synthesis in the periimplantation stroma and the capacity to quickly up-regulate focal VEGF secretion needed to induce early angiogenic events of pregnancy.

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