Aggravation of atherosclerosis by pulmonary exposure to indium oxide nanoparticles

Lee, Jaewoong; Jang, Hyonchol; Chung, Hyunji; Jeon, Soyeon; Jeong, Jinho; Choi, Jae Hoon; Cho, Wan Seob

doi:10.1080/17435390.2019.1704590

Cited by 13 publications

(8 citation statements)

References 41 publications

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“…The low-density lipoprotein (LDL) receptor (LDLR) binds both LDL and haptoglobin [ 193 ]. A recent study used Ldlr KO mice to examine systemic inflammation caused by indium dioxide (In 2 O 3 ) nanoparticles.…”

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

“…A recent study used Ldlr KO mice to examine systemic inflammation caused by indium dioxide (In 2 O 3 ) nanoparticles. After a single pharyngeal aspiration dose of In 2 O 3 nanoparticles, Ldlr KO mice developed significantly severe atherosclerotic lesions compared to wild type mice [ 193 ]. The Ldlr KO mice also showed that the aorta had a much higher transcript level of IL-6 and MCP-1 (CCL2), suggesting ongoing inflammation in the heart [ 193 ].…”

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

“…After a single pharyngeal aspiration dose of In 2 O 3 nanoparticles, Ldlr KO mice developed significantly severe atherosclerotic lesions compared to wild type mice [ 193 ]. The Ldlr KO mice also showed that the aorta had a much higher transcript level of IL-6 and MCP-1 (CCL2), suggesting ongoing inflammation in the heart [ 193 ]. Ldlr KO mice also showed an increase in total cholesterol and low-density lipoprotein in the plasma compared to wild type mice after treatment [ 193 ].…”

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

“…The Ldlr KO mice also showed that the aorta had a much higher transcript level of IL-6 and MCP-1 (CCL2), suggesting ongoing inflammation in the heart [ 193 ]. Ldlr KO mice also showed an increase in total cholesterol and low-density lipoprotein in the plasma compared to wild type mice after treatment [ 193 ]. Therefore, this study emphasized the protective role of the LDLR in limiting cardiovascular disease after pulmonary exposure to an ENM.…”

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

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Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials

You

Bonner

2020

IJMS

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Engineered nanomaterials (ENMs) are products of the emerging nanotechnology industry and many different types of ENMs have been shown to cause chronic inflammation in the lungs of rodents after inhalation exposure, suggesting a risk to human health. Due to the increasing demand and use of ENMs in a variety of products, a careful evaluation of the risks to human health is urgently needed. An assessment of the immunotoxicity of ENMs should consider susceptibility factors including sex, pre-existing diseases, deficiency of specific genes encoding proteins involved in the innate or adaptive immune response, and co-exposures to other chemicals. This review will address evidence from experimental animal models that highlights some important issues of susceptibility to chronic lung inflammation and systemic immune dysfunction after pulmonary exposure to ENMs.

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Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

Section: Susceptible Organ Systems and Pre-existing Disease Statesmentioning

confidence: 99%

See 2 more Smart Citations

Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials

You

Bonner

2020

IJMS

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“…Inhalation of engineered NPs such as TiO 2 NPs, single-walled carbon nanotubes (SWCNTs) and nickel hydroxide NPs (nano-Ni), etc. could accelerate the pathological progress of atherosclerosis [20][21][22][23]. But some engineered NPs such as selenium and copper sul de NPs were reported to antagonize atherosclerosis [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE-/- mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Zhao

et al. 2020

Preprint

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Abstract Background: The biosafety concern of silica nanoparticles (SiNPs) is rapidly expanding alongside with its mass production and extensive applications. The cardiovascular effects of SiNPs exposure have been confirmed. However, the interaction between SiNPs exposure and atherosclerosis, and the underlying mechanisms still remain unknown. Thereby, this study aimed to explore the effects of SiNPs on the progression of atherosclerosis, and to investigate related mechanisms. Results: We firstly investigated the in vivo effects of SiNPs exposure on atherosclerosis via intratracheal instillation of ApoE -/- mice fed a Western diet. Ultrasound microscopy showed a significant increase of pulse wave velocity (PWV) compared to the control group. Histopathological investigation reflected a greater plaque burden in the aortic root of SiNPs-exposed ApoE -/- mice. When compared to the control, serum levels of total triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) were elevated after SiNPs exposure. Moreover, intensified macrophage infiltration and endoplasmic reticulum (ER) stress was occurred in plaques after SiNPs exposure, as evidenced by the upregulated CD68 and CHOP expressions. Further in vitro , SiNPs was confirmed to activate ER stress and induce lipid accumulation in mouse macrophage, RAW264.7. Mechanistic analyses showed that 4-PBA (a classic ER stress inhibitor) pretreatment greatly alleviated SiNPs-induced macrophage lipid accumulation, and reversed the elevated CD36 expression by SiNPs. Conclusions: Our results firstly revealed the acceleratory effect of SiNPs on the progression of atherosclerosis in ApoE -/- mice, which was related to lipid accumulation caused by ER stress-mediated upregulation of CD36 expression in macrophage.

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Potential roles of Kruppel‐like factors in mediating adverse vascular effects of nanomaterials: A review

Cao

2021

J of Applied Toxicology

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The development of nanotechnology leads to the exposure of human beings to nanomaterials (NMs), and there is a health concern about the adverse vascular effects of NMs. Current data from epidemiology, controlled human exposure, and animal studies suggested that exposure to NMs could induce cardiopulmonary effects. In support of in vivo findings, in vitro studies showed that direct contact of vascular cells with NMs could induce endothelial cell (EC) activation and promote macrophage foam cell formation, although only limited studies showed that NMs could damage vascular smooth muscle cells and promote their phenotypic switch. It has been proposed that NMs induced adverse vascular effects via different mechanisms, but it is still necessary to understand the upstream events. Kruppel‐like factors (KLFs) are a set of C2H2 zinc finger transcription factors (TFs) that can regulate various aspects of vascular biology, but currently, the roles of KLF2 in mediating the adverse vascular effects of NMs have gained little attention by toxicologists. This review summarized current knowledge about the adverse vascular effects of NMs and proposed the potential roles of KLFs in mediating these effects based on available data from toxicological studies as well as the current understanding about KLFs in vascular biology. Finally, the challenges in investigating the role of KLFs in vascular toxicology were also summarized. Considering the important roles of KLFs in vascular biology, further studies are needed to understand the influence of NMs on KLFs and the downstream events.

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Aggravation of atherosclerosis by pulmonary exposure to indium oxide nanoparticles

Cited by 13 publications

References 41 publications

Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials

Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials

Amorphous silica nanoparticles accelerated atherosclerotic lesion progression in ApoE-/- mice through endoplasmic reticulum stress-mediated CD36 up-regulation in macrophage

Potential roles of Kruppel‐like factors in mediating adverse vascular effects of nanomaterials: A review

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