A Water-Soluble Fullerene Vesicle Alleviates Angiotensin II-Induced Oxidative Stress in Human Umbilical Venous Endothelial Cells

Maeda, Ryo; Noiri, Eisei; Isobe, Hiroyuki; Homma, Tatsuya; Tanaka, Tamami; Negishi, Kousuke; Doi, Kent; Fujita, Toshiro; Nakamura, Eiichi

doi:10.1291/hypres.31.141

Cited by 37 publications

(19 citation statements)

References 53 publications

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“…Although these injury markers demonstrate the organ injury and its severity, further investigation is necessary to clarify the mechanism of toxicity by Lipofectin. Several previous reports described no evidence of toxicity by fullerene (29)(30)(31). On the other hand, cationic liposome is reported to have toxicity (9,26,32).…”

Section: Discussionmentioning

confidence: 91%

In vivo gene delivery by cationic tetraamino fullerene

Maeda-Mamiya

Noiri

Isobe

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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164

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Application of nanotechnology to medical biology has brought remarkable success. Water-soluble fullerenes are molecules with great potential for biological use because they can endow unique characteristics of amphipathic property and form a self-assembled structure by chemical modification. Effective gene delivery in vitro with tetra(piperazino)fullerene epoxide (TPFE) and its superiority to Lipofectin have been described in a previous report. For this study, we evaluated the efficacy of in vivo gene delivery by TPFE. Delivery of enhanced green fluorescent protein gene (EGFP) by TPFE on pregnant female ICR mice showed distinct organ selectivity compared with Lipofectin; moreover, higher gene expression by TPFE was found in liver and spleen, but not in the lung. No acute toxicity of TPFE was found for the liver and kidney, although Lipofectin significantly increased liver enzymes and blood urea nitrogen. In fetal tissues, neither TPFE nor Lipofectin induced EGFP gene expression. Delivery of insulin 2 gene to female C57/BL6 mice increased plasma insulin levels and reduced blood glucose concentrations, indicating the potential of TPFE-based gene delivery for clinical application. In conclusion, this study demonstrated effective gene delivery in vivo for the first time using a water-soluble fullerene.

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Section: Discussionmentioning

confidence: 91%

In vivo gene delivery by cationic tetraamino fullerene

Maeda-Mamiya

Noiri

Isobe

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

164

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“…Recently, some studies have focused on exploring the effect of Ang II on endothelial cells [27,28,29,30]. Moreover, the role of Ang II in mediating HUVEC responses to oxidative stress has been investigated [31,32]. Although past studies have confirmed that EGCG inhibits Ang II-induced adhesion molecule levels in HUVECs [33,34], understanding of the underlying molecular mechanisms remains limited.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

et al. 2017

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Introduction: This study aimed to investigate whether epigallocatechin-3-gallate (EGCG) shows antioxidant activity against angiotensin II (Ang II)-induced human umbilical vein endothelial cell (HUVEC) apoptosis. Materials and Methods: The viability of HUVECs was revealed by MTT and LDH assay. The cell apoptosis was detected by FITC-PI assay. A fluorescent probe assay was used to measure the reactive oxygen species (ROS) generation in HUVECs. Mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential, and caspase-3, -4, -8, -9 activities were also measured. Results: We found that Ang II treatment increased the generation of ROS, enhanced MPTP opening and cytochrome c release, activated caspase-3/9, and consequently induced HUVEC apoptosis. EGCG treatment-suppressed Ang II induces the oxidative stress of HUVECs and mitochondria-related cell apoptosis. We also showed that the antioxidant activity pathway, including cytochrome c release, MPTP opening, and caspase-3/9 activation, is a key endogenous defensive system in HUVECs, provoking Ang II exposure. Our study revealed that increased expression of Nrf2 by EGCG could partially repress Ang II-induced injury effects. Conclusions: All of our findings indicated that EGCG treatment provides a protective effect for Ang II-induced HUVEC apoptosis by decreasing oxidative stress and ameliorating mitochondrial injury.

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“…This is due to the relatively large number of conjugated double bonds in the fullerene molecule, which can be attacked by radical species. Thus, fullerenes would be suitable for applications in quenching oxygen radicals, and thus preventing inflammatory and allergic reactions (Dellinger et al, 2009) and damage of various tissues and organs, including the lung (Chen et al, 2004), blood vessels (Maeda et al, 2008) and brain (Tykhomyrov et al, 2008;Lao et al, 2009). Fullerenes also protected epithelial cells in vitro from anoikis, i.e., apoptosis due to adhesion deprivation, by a mechanism supporting the formation of focal adhesion plaques, assembly of the actin cytoskeleton and cell spreading, which was also attributed to the antioxidative action of fullerenes (Straface et al, 1999).…”

Section: Fullerenesmentioning

confidence: 99%