摘要：
Despite of growing evidence linking PM(2.5) exposure to autophagic activity in various human cells, the functional significance of PM(2.5) exposure affecting autophagy in the pathogenesis of human cardiovascular disease and the underlying molecular mechanisms remain unclear. In this study, the effects of ambient PM(2.5) (with final concentration 0, 1, 5, 25µg/mL) on the autophagic activity in human umbilical vein endothelial cells (HUVECs) were systematically studied. The results showed that the internalized PM(2.5) mainly localized in the membrane-surrounded vacuoles in the cytoplasm. Compared with the negative control, dose-dependent increase of autophagosomes, puncta and protein levels of LC3-II and p62, and both dose- and time-dependent increase of AKT phosphorylation, with inversely time-dependent reduction of Beclin 1, ATG3 and ATG5 proteins, were presented in the PM(2.5)-treated HUVECs, indicating a clear impairment of autophagic degradation in the PM(2.5)-exposed HUVECs. Meanwhile, increase in lysosomes, LAMP1, proteases of CTSB and CTSD, and protein phosphorylation of ERK1/2 and TFEB was identified in the PM(2.5)-treated HUVECs, showing a PM(2.5)-mediated enhancement in lysosomal activity. A novel finding in this study is that both Sntaxin-17 and LAMP2, two key proteins involved in the control of membrane fusion between autophagosome and lysosome, were significantly decreased in the PM(2.5)-exposed HUVECs, suggesting that the fusion of autophagosome-lysosome was blocked up. Collectively, ambient PM(2.5) exposure may block up the autophagic flux in HUVECs through inhibiting the expression of Sntaxin-17 and LAMP2. Autophagic activity in HUVECs is a useful biomarker for assessing risks of environmental factors to human cardiovascular health.
摘要：
Radiation-induced pulmonary fibrosis (RIPF) is a major lung complication in using radiotherapy to treat thoracic diseases. MicroRNAs (miRNAs) are reported to be the therapeutic targets for many diseases. However, the miRNAs involved in the pathogenesis of RIPF are rarely studied as potential therapeutic targets. Alveolar epithelial cells participate in RIPF formation by undergoing epithelial-mesenchymal transition (EMT). Here we demonstrated the critical role of miR-155-5p in radiation-induced EMT and RIPF. Using the previously established EMT cell model, we found that miR-155-5p was significantly down-regulated through high-throughput sequencing. Irradiation could decrease the expression of miR-155-5p in intro and in vivo, and it was inversely correlated to RIPF formation. Ectopic miR-155-5p expression inhibited radiation-induced-EMT in vitro and in vivo. Knockdown of glycogen synthase kinase-3 beta (GSK-3 beta), the functional target of miR-155-5p, reversed the induction of EMT and enhanced the phosphorylation of p65, a subunit of NF-kappa B, which were mediated by the down-regulation of miR-155-5p. Moreover, our finding demonstrated that ectopic miR-155-5p expression alleviated RIPF in mice by the GSK-3 beta/NF-kappa B pathway. Thus, radiation downregulates miR-155-5p in alveolar epithelial cells that induces EMT, which contributes to RIPF using GSK-3 beta/NF-kappa B pathway. Our observation provides further understanding on the regulation of RIPF and identifies potential therapeutic targets.
通讯机构：
[He, Shu-Ya; Peng, Guo-Wen] U;Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.;Univ South China, Sch Chem & Chem Engn, Hengyang 421001, Peoples R China.;Univ South China, Sch Resource Environm & Safety Engn, Hengyang 421001, Peoples R China.;Univ South China, Hunan Prov Engn Technol Res Ctr Uranium Tailings, Hengyang 421001, Peoples R China.
关键词：
calixarene, Fe3O4, magnetic materials, separation.
摘要：
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Environmental contextUranium-containing wastewaters have high potential to harm the environment and human health. We found that the combination of calix[4]arene with magnetic Fe3O4 particles produced good adsorption of uranium from wastewater. In addition, this material can be recycled and reused, so it has good prospects in practical applications for uranium remediation.
AbstractA magnetic functionalised calix[4]arene composite consisting of Fe3O4 and calix[4]arene phosphonate derivative (CPD) was prepared through a facile self-assembly method. The composite was characterised by scanning electron microscopy (SEM), powder X-ray diffraction (PXRD) and Fourier transform infrared spectroscopy (FTIR). The as-synthesised Fe3O4/CPD composite was used to remove UVI from aqueous solutions under different conditions. Meanwhile, the adsorption isotherm, kinetics and thermodynamics were fitted and analysed. The results show that the Fe3O4/CPD composite may be a promising adsorption material for the separation and enrichment of UVI from aqueous solutions in the cleanup of environmental pollution.
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摘要：
Despite intensive research activities, there are still many major knowledge gaps over the potential adverse effects of titanium dioxide nanoparticles (TiO2-NPs), one of the most widely produced and used nanoparticles, on human cardiovascular health and the underlying mechanisms. In the present study, alkaline comet assay and cytokinesis-block micronucleus test were employed to determine the genotoxic potentials of four sizes (100, 50, 30, and 10 nm) of anatase TiO2-NPs to human umbilical vein endothelial cells (HUVECs) in culture. Also, the intracellular redox statuses were explored through the measurement of the levels of reactive oxygen species (ROS) and reduced glutathione (GSH) with kits, respectively. Meanwhile, the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) were also detected by western blot. The results showed that at the exposed levels (1, 5, and 25 mu g/mL), all the four sizes of TiO2-NPs could elicit an increase of both DNA damage and MN frequency in HUVECs in culture, with a positive dose-dependent and negative size-dependent effect relationship (T100 < T50 < T30 < T10). Also, increased levels of intracellular ROS, but decreased levels of GSH, were found in all the TiO2-NP-treated groups. Intriguingly, a very similar manner of dose-dependent and size-dependent effect relationship was observed between the ROS test and both comet assay and MN test, but contrary to that of GSH assay. Correspondingly, the levels of Nrf2 protein were also elevated in the TiO2-NP-exposed HUVECs, with an inversely size-dependent effect relationship. These findings indicated that induction of oxidative stress and subsequent genotoxicity might be an important biological mechanism by which TiO2-NP exposure would cause detrimental effects to human cardiovascular health.
摘要：
<jats:title>Abstract</jats:title><jats:p>Concerns over the health risk of the widely distributed, commonly used titanium dioxide nanoparticles (nano‐TiO<jats:sub>2</jats:sub>) are increasing worldwide. Yet, up‐to‐now, our understanding in their potential effects on the cardiovascular system is very limited and the toxicological mechanisms are still unclear. In the present study, the CCK‐8 assay was performed to determine the cytotoxicity of four sizes (10, 30, 50, and 100 nm) of anatase nano‐TiO<jats:sub>2</jats:sub> on human umbilical vein endothelial cells (HUVECs) in culture, and the flow cytometry was employed to investigate the potential of these nano‐TiO<jats:sub>2</jats:sub> to induce the apoptosis of HUVECs. The apoptotic pathway was also probed through the determination of the protein expression and activation of p53, Bax, Bcl‐2, caspases‐9, ‐7, ‐3, and PARP by western blot. The results showed that at the administrative levels (1, 5, 25 μg/mL), all the four sizes of nano‐TiO<jats:sub>2</jats:sub> could significantly inhibit the viability of HUVECs and elicit significant apoptosis in them, compared with the negative control (<jats:italic>P</jats:italic> < .05, <jats:italic>P</jats:italic> < .01). Moreover, the apoptotic rates of HUVECs were increased respectively with the elevating levels and decreasing sizes of the administrative nano‐TiO<jats:sub>2</jats:sub>, showing a clear dose‐ and size‐dependent effect relationships. Interestingly, the increasing phosphorylation of p53, decreasing ratio of Bcl‐2/Bax, and enhancing activation of the downstream proteins caspase‐9, ‐7, ‐3, and PARP, were also observed with the decreasing sizes of the administrative nano‐TiO<jats:sub>2</jats:sub> in the western blot, indicating that the intracellular approach of apoptosis, the p53‐caspase pathway, is the major way of the nano‐TiO<jats:sub>2</jats:sub>‐mediated apoptosis in HUVECs in culture and that the size is an important parameter that may determine the potential of nano‐TiO<jats:sub>2</jats:sub> to induce cellular response. In conclusion, these results suggested that high levels of nano‐TiO<jats:sub>2</jats:sub> exposure may pose potential risks to human cardiovascular health by inducing cardiovascular EC apoptosis.</jats:p>
摘要：
<ce:abstract xmlns:ce="" xmlns="" xml:lang="en" id="abs0010" view="all" class="author"><ce:section-title id="sectitle0010">Abstract</ce:section-title><ce:abstract-sec id="abssec0010" view="all"><ce:simple-para id="abspara0010" view="all">With the growing production and applications of silica nanoparticles (SiNPs), human exposure to these nanoparticles continues to increase. However, the possible hazards that SiNP exposure may pose to human cardiovascular system and the underlying mechanisms remain unclear. In the present study, the flow cytometry was employed to investigate the potential of four sizes (10, 25, 50, 100?nm) of SiNPs to induce the apoptosis of human umbilical vein endothelial cells (HUVECs) in culture. The apoptotic pathway was also explored through the determination of the protein expression and/or activation of p53, Bcl-2, Bax, caspases-9, -7, -3, and PARP by western blot. The results showed that all the four sizes of SiNPs could significantly elicit apoptosis in HUVECs at the tested concentrations (1, 5, 25?μg/mL), compared with the negative control (p?<?0.05, p?<?0.01). Moreover, the apoptotic rates were increased with the elevating levels and decreasing sizes of administrative SiNPs, showing both dose- and size-dependent effect relationships. Interestingly, the enhancing phosphorylation of p53 protein (Ser15), decreasing ratio of Bcl-2/Bax protein, and elevating activation of the downstream proteins, caspase-9, -7, -3 and PARP, were also observed with the decreasing sizes of tested SiNPs, indicating that the p53-caspase pathway is the main way of the SiNP-mediated apoptosis in HUVECs and that the size is an important parameter that determines the SiNPs' potential to induce cellular response.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:abstract xmlns:ce="" xmlns="" class="graphical" id="abs0015" view="all"><ce:section-title id="sectitle0015">Graphical abstract</ce:section-title><ce:abstract-sec id="abssec0015" view="all"><ce:simple-para>Display Omitted</ce:simple-para></ce:abstract-sec></ce:abstract><ce:abstract xmlns:ce="" xmlns="" class="author-highlights" xml:lang="en" id="abs0020" view="all"><ce:section-title id="sectitle0020">Highlights</ce:section-title><ce:abstract-sec id="abssec0020" view="all"><ce:simple-para id="abspara0020" view="all"><ce:list id="ulist0010"><ce:list-item id="u0010"><ce:label>?</ce:label><ce:para id="p0010" view="all">This study explored the apoptotic effects of SiNPs on endothelial cells and underlying molecular mechanism.</ce:para></ce:list-item><ce:list-item id="u0015"><ce:label>?</ce:label><ce:para id="p0015" view="all">The SiNPs may cause significant apoptosis to HUVECs in culture, with a clear dose- and size-dependent effect relationships.</ce:para></ce:list-item><ce:list-item id="u0020"><ce:label>?</ce:label><ce:para id="p0020" view="all">SiNP exposure may pose potential risks to human cardiovascular health via inducing EC apoptosis by the p53-caspase pathway.</ce:para></ce:list-item><ce:list-item id="u0025"><ce:label>?</ce:label><ce:para id="p0025" view="all">The size is an important parameter that determines SiNPs' potential to elicit cellular responses.</ce:para></ce:list-item></ce:list></ce:simple-para></ce:abstract-sec></ce:abstract><ce:abstract xmlns:ce="" xmlns="" class="teaser" id="abs0025" view="all"><ce:abstract-sec id="abssec0025" view="all"><ce:simple-para i
期刊：
Journal of Radioanalytical and Nuclear Chemistry,2017年314(3):2137-2143 ISSN：0236-5731
通讯作者：
Peng, Guo-wen
作者机构：
[Peng, Guo-wen; Wang, Cheng; Pu, Yi-qiu] Univ South China, Sch Chem & Chem Engn, Hengyang 421001, Hunan, Peoples R China.;[He, Suya; Xiao, Fangzhu] Univ South China, Sch Publ Hlth, Hengyang 421001, Hunan, Peoples R China.;[Peng, Guo-wen; Liu, Yong] Univ South China, Hu Nan Prov Engn Technol Res Ctr UraniumTailings, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Peng, Guo-wen] U;Univ South China, Sch Chem & Chem Engn, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Hu Nan Prov Engn Technol Res Ctr UraniumTailings, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Long, Dingxin] U;[Chen, Chunying] N;Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.;Natl Ctr Nanosci & Technol China, CAS Key Lab Biomed Effects Nanomat & Nanosafety, Beijing 100190, Peoples R China.;Natl Ctr Nanosci & Technol China, CAS Ctr Excellence Nanosci, Beijing 100190, Peoples R China.
摘要：
Concerns have arisen about the health and environmental impacts of the increasing commercial use of silver nanoparticles (AgNPs). However, the toxic mechanisms and target tissues of AgNPs have not been fully defined. In this paper, we investigated the tissue toxicity of mice after intravenous administration of AgNPs at a single-dose of 0.2, 2 or 5 mg per kg (body weight), respectively. Biodistribution, endoplasmic reticulum stress, and oxidative stress were examined in mouse organs at eight hours after exposure. Stress markers, e.g. HSP70, BIP, p-IRE1, p-PERK, chop and xbp-1s proteins/genes, were significantly upregulated in a dose-dependent manner. In the liver, spleen, lung and kidney, high stress accompanied by apoptosis occurred. Low stress levels were observed in the heart and brain. Thus, it is proposed that the liver, spleen, lung and kidney are dominant target tissues of AgNP exposure. The lower stress and toxicity in the heart and brain were in agreement with lower AgNP accumulation. The present results demonstrated that AgNP exposure eventually resulted in permanent toxic damage by gradually imposing stress impacts on target organs. These findings highlight the potent applications of stress markers in future risk evaluation of silver nanoparticle toxicity.
通讯机构：
[Tan, Weihong] U;Univ Florida, Dept Chem, Ctr Res Bio Nano Interface, Gainesville, FL 32611 USA.
摘要：
A facile strategy has been developed to fabricate Cu(OH)(2) supercages (SCs) as an artificial enzyme system with intrinsic peroxidase-mimic activities (PMA). SCs with high catalytic activity and excellent recyclability were generated via direct conversion of amorphous Cu(OH)(2) nanoparticles (NPs) at room temperature. More specifically, the process that takes a single nanoparticle to a 3D supercage involves two basic steps. First, with addition of a copper ammonia complex, the Cu2+ ions that are located on the surface of amorphous Cu(OH)(2) NPs would evolve into a fine lamellar structure by coordination and migration and eventually convert to ID nanoribbons around the NPs. Second, accompanied by the migration of Cu2+, a hollow cavity is generated in the inner NPs, such that a single nanoparticle eventually becomes a nanoribbon-assembled 3D hollow cage. These Cu(OH)(2) SCs were then engineered as an artificial enzymatic system with higher efficiency for intrinsic PMA than the peroxidase activity of a natural enzyme, horseradish peroxidase.
作者机构：
[Yu, M. J.; Tang, S. Y.; Liu, A. Y.; Liu, Y.; Liu, L. Z.; Wan, Y. P.; Zhang, Y.] Univ South China, Pathogen Biol Inst, Hengyang 421001, Peoples R China.;[Li, L.] Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.
通讯机构：
[Tang, S. Y.] U;Univ South China, Pathogen Biol Inst, Hengyang 421001, Peoples R China.
关键词：
human papillomavirus type16 (HPV16);E2;Daxx;interaction
