Comprehensive Analysis of SiNPs on the Genome-Wide Transcriptional Changes in .

Background: Large-scale production and application of amorphous silica nanoparticles (SiNPs) have enhanced the risk of human exposure to SiNPs. However, the toxic effects and the underlying biological mechanisms of SiNPs on remain largely unclear.

Purpose: This study was to investigate the genome-wide transcriptional alteration of SiNPs on .

Repeat dose exposure of PM triggers the disseminated intravascular coagulation (DIC) in SD rats.

Epidemiological evidence suggests that fine particulate matter (PM) in air pollution promotes the formation of deep venous thrombosis. However, no evidence is available on the effects of PM lead to disseminated intravascular coagulation (DIC). For the first time, this study explored the effects of PM on DIC via coagulation disorders in vivo.

Gene profiles to characterize the combined toxicity induced by low level co-exposure of silica nanoparticles and benzo[a]pyrene using whole genome microarrays in zebrafish embryos.

Several studies have suggested that air pollutants combine exposure have greater adverse effects. However, limited studies were available on the combined toxicity of silica nanoparticles (SiNPs) and benzo[a]pyrene (B[a]P). The study was to evaluate the toxic effect and mechanisms of low-dose exposure of SiNPs, B[a]P and co-exposure in zebrafish embryos.

Co-exposure of silica nanoparticles and methylmercury induced cardiac toxicity in vitro and in vivo.

The released nanoparticles into environment can potentially interact with pre-existing pollution, maybe causing higher toxicity. As such, assessment of their joint toxic effects is necessary. This study was to investigate the co-exposure cardiac toxicity of silica nanoparticles (SiNPs) and methylmercury (MeHg).

Low-dose combined exposure of nanoparticles and heavy metal compared with PM in human myocardial AC16 cells.

The co-exposure toxicity mechanism of ultrafine particles and pollutants on human cardiovascular system are still unclear. In this study, the combined effects of silica nanoparticles (SiNPs) and/or carbon black nanoparticles (CBNPs) with Pb(AC) compared with particulate matter (PM) were investigated in human myocardial cells (AC16). Our study detected three different combinations of SiNPs and Pb(AC), CBNPs and Pb(AC), and SiNPs and CBNPs compared with PM at low-dose exposure.

Cellular pathways involved in silica nanoparticles induced apoptosis: A systematic review of in vitro studies.

Silica nanoparticles (SiNPs) have been found to pass through biological barriers and get distributed in the human body. They induce cell apoptosis via various mechanisms in body organs. To understand these mechanisms, we carried out systematic review of in vitro studies on SiNPs-induced cell apoptosis.

Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells.

There is compelling evidence that exposure to particulate matter (PM) is linked to lung tumorigenesis. However, there is not enough experimental evidence to support the specific mechanisms of PM-induced DNA damage and cell cycle arrest in lung tumorigenesis. In this study, we investigated the toxic effects and molecular mechanisms of PM on bronchial epithelial (BEAS-2B) cells.

Comprehensive gene and microRNA expression profiling on cardiovascular system in zebrafish co-exposured of SiNPs and MeHg.

Air pollution has been shown to increase cardiovascular diseases. However, little attention has been paid to the combined effects of PM and air pollutants on the cardiovascular system. To explore this, a high-throughput sequencing technology was used to determine combined effects of silica nanoparticles (SiNPs) and MeHg in zebrafish.

Microarray-based bioinformatics analysis of the combined effects of SiNPs and PbAc on cardiovascular system in zebrafish.

With rapid development of nanotechnology and growing environmental pollution, the combined toxic effects of SiNPs and pollutants of heavy metals like lead have received global attentions. The aim of this study was to explore the cardiovascular effects of the co-exposure of SiNPs and lead acetate (PbAc) in zebrafish using microarray and bioinformatics analysis. Although there was no other obvious cardiovascular malformation except bleeding phenotype, bradycardia, angiogenesis inhibition and declined cardiac output in zebrafish co-exposed of SiNPs and PbAc at NOAEL level, significant changes were observed in mRNA and microRNA (miRNA) expression patterns.

Gene expression profiles and bioinformatics analysis of human umbilical vein endothelial cells exposed to PM.

Cardiovascular system is demonstrated the main target of PM and the objective of this study was to explore the toxic effect and molecular mechanisms caused by PM in primary human umbilical vein endothelial cells (HUVECs) using microarray and bioinformatics analysis. The results showed that 591 genes were differentially expressed triggered by PM, of which 174 genes were down-regulated, while 417 genes were up-regulated. Gene ontology analysis revealed that PM caused significant changes in gene expression patterns, including response to stimuli, immune response, and cellular processes.

Silica nanoparticles inhibit macrophage activity and angiogenesis via VEGFR2-mediated MAPK signaling pathway in zebrafish embryos.

The safety evaluation of silica nanoparticles (SiNPs) are getting great attention due to its widely-used in food sciences, chemical industry and biomedicine. However, the adverse effect and underlying mechanisms of SiNPs on cardiovascular system, especially on angiogenesis is still unclear. This study was aimed to illuminate the possible mechanisms of SiNPs on angiogenesis in zebrafish transgenic lines, Tg(fli-1:EGFP) and Albino.

Multi-organ toxicity induced by fine particulate matter PM in zebrafish (Danio rerio) model.

The fine particulate matter (PM) in air pollution is a major public health concern and now known to contribute to severe diseases, therefore, a comprehensive understanding of PM-induced adverse effects in living organisms is needed urgently. This study was aimed to evaluate the toxicity of PM on multi-organ systems in a zebrafish (Danio rerio) model. The embryonic toxicity induced by PM was demonstrated by an increase in mortality and inhibition of hatching rate, in a dose- and time-dependent manner.

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM in human myocardial cells.

Air pollution has been a major environment-related health threat. Most of the studies on PM toxicity have verified on the cardiovascular system and endothelial cells. However, researches on PM-induced myocardial-related toxicity are limited.

Combined Effect of Silica Nanoparticles and Benzo[a]pyrene on Cell Cycle Arrest Induction and Apoptosis in Human Umbilical Vein Endothelial Cells.

Particulate matter (PM) such as ultrafine particulate matter (UFP) and the organic compound pollutants such as polycyclic aromatic hydrocarbon (PAH) are widespread in the environment. UFP and PAH are present in the air, and their presence may enhance their individual adverse effects on human health. However, the mechanism and effect of their combined interactions on human cells are not well understood.

H NMR-based metabolomics study on repeat dose toxicity of fine particulate matter in rats after intratracheal instillation.

Systemic metabolic effects and toxicity mechanisms of ambient fine particulate matter (PM) remain uncertain. In order to investigate the mechanisms in PM toxicity, we explored the endogenous metabolic changes and possible influenced metabolic pathways in rats after intratracheal instillation of PM by using a H nuclear magnetic resonance (NMR)-based metabolomics approach. Liver and kidney histopathology examinations were also performed.

Co-exposure to amorphous silica nanoparticles and benzo[a]pyrene at low level in human bronchial epithelial BEAS-2B cells.

Both ultrafine particles (UFP) and polycyclic aromatic hydrocarbons (PAHs) are widely present in the environment, thus increasing their chances of exposure to human in the daily life. However, the study on the combined toxicity of UFP and PAHs on respiratory system is still limited. In this study, we examined the potential interactive effects of silica nanoparticles (SiNPs) and benzo[a]pyrene (B[a]P) in bronchial epithelial cells (BEAS-2B).

Cytotoxicity and autophagy dysfunction induced by different sizes of silica particles in human bronchial epithelial BEAS-2B cells.

The adverse effects of silica nanoparticles are gaining attention due to their wide application in biomedicine. However, information about size-dependent toxicity induced by silica nanoparticles is insufficient. In this study, two size of nano-scale (40 nm, 60 nm) and one size of micro-scale (200 nm) silica particles were studied to investigate the possible mechanism of cytotoxicity and autophagy dysfunction in human bronchial epithelial BEAS-2B cells.

Combined toxicity of silica nanoparticles and methylmercury on cardiovascular system in zebrafish (Danio rerio) embryos.

This study was to investigate the combined toxicity of silica nanoparticles (SiNPs) and methylmercury (MeHg) on cardiovascular system in zebrafish (Danio rerio) embryos. Ultraviolet absorption analysis showed that the co-exposure system had high absorption and stability. The dosages used in this study were based on the NOAEL level.

Fine particulate matter induces vascular endothelial activation IL-6 dependent JAK1/STAT3 signaling pathway.

Exposure to PM2.5 has been strongly linked to endothelial dysfunction. However, the underlying mechanism of PM2.