Safety of Nonporous Silica Nanoparticles in Human Corneal Endothelial Cells

Kim, Ja Yeon; Park, Joo Hee; Kim, Martha; Jeong, Hyejoong; Hong, Jinkee; Chuck, Roy S.; Park, Keun

doi:10.1038/s41598-017-15247-2

Cited by 29 publications

(17 citation statements)

References 49 publications

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“…Interestingly, the toxicity and the therapeutic effect observed might be derived from the modulation of the autophagy. For instance, Si-NPs have been shown to induce cytotoxicity and autophagy cell death on human umbilical vein, cerebral and corneal endothelial cells through several mechanisms, including ROS generation, dysregulation of PI3K/Akt/mTOR pathway, by affecting angiogenesis and cellular homeostasis, and by leading mitochondrial instability and mitophagy [ 192 – 196 ]. Si-NPs, depending on their size, have also been shown to induce cytotoxicity and autophagy dysfunction in human bronchial epithelial BEAS-2B cells [ 197 ].…”

Section: Other Examples Of Autophagy Modulation Using Nanoparticlesmentioning

confidence: 99%

Targeting autophagy using metallic nanoparticles: a promising strategy for cancer treatment

Cordani

Somoza

2018

Cell. Mol. Life Sci.

156

105

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Despite the extensive genetic and phenotypic variations present in the different tumors, they frequently share common metabolic alterations, such as autophagy. Autophagy is a self-degradative process in response to stresses by which damaged macromolecules and organelles are targeted by autophagic vesicles to lysosomes and then eliminated. It is known that autophagy dysfunctions can promote tumorigenesis and cancer development, but, interestingly, its overstimulation by cytotoxic drugs may also induce cell death and chemosensitivity. For this reason, the possibility to modulate autophagy may represent a valid therapeutic approach to treat different types of cancers and a variety of clinical trials, using autophagy modulators, are currently employed. On the other hand, recent progress in nanotechnology offers plenty of tools to fight cancer with innovative and efficient therapeutic agents by overcoming obstacles usually encountered with traditional drugs. Interestingly, nanomaterials can modulate autophagy and have been exploited as therapeutic agents against cancer. In this article, we summarize the most recent advances in the application of metallic nanostructures as potent modulators of autophagy process through multiple mechanisms, stressing their therapeutic implications in cancer diseases. For this reason, we believe that autophagy modulation with nanoparticle-based strategies would acquire clinical relevance in the near future, as a complementary therapy for the treatment of cancers and other diseases.

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Section: Other Examples Of Autophagy Modulation Using Nanoparticlesmentioning

confidence: 99%

Targeting autophagy using metallic nanoparticles: a promising strategy for cancer treatment

Cordani

Somoza

2018

Cell. Mol. Life Sci.

156

105

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“…28 SiNPs could be uptaken by the cells which in turn causes inflammation due to the production of inflammatory factors; this further results in the injury to vascular system physically and chemically. 29 Blood toxicity in SiNPs-induced mice results in oxidative stress damage which was shown to be the reason for their noxious effect. 30 In rat cardiomyocyte (H9c2) cell line, SiNPs also reduced gap junction intercellular communication, which is one of the targets for biological effects through upregulation of p-Cx43.…”

Section: 200 On 29-sep-2020mentioning

confidence: 99%

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Lin

Yang

Shi

et al. 2018

IJN

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BackgroundThe harmful effects following the release of nanomaterials into environment are of great concern today.PurposeIn this study, subacute effect due to co-exposure to low-dose silica nanoparticles (SiNPs) and lead acetate (Pb) on cardiovascular system was detected in Sprague Dawley male rats.Materials and MethodsHistopathological and ultrastructural changes of heart, aortic arch and abdominal aorta were detected. Blood routine and blood biochemistry examinations were used to show the changes of blood components. The fibrinolytic and plasmin factors, inflammation-related factors and myocardial-related enzyme in serum were analysised by ELISA and Western blot assay.ResultsHistopathological and ultrastructural examination of heart, aortic arch, and abdominal aorta showed that serious damage occurred in co-exposure group (n=6/group). Blood routine examination showed that leukocytosis and thrombocytopenia increased markedly, while changes in the erythrocyte count were not obvious in the co-exposure group. The expression of alanine transaminase (ALT) decreased obviously in co-exposure group, while no significant changes were noted in the expression of aspartate aminotransferase (AST), cholesterol (CHO), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) in the co-exposure group on blood biochemistry analysis. In addition, data from ELISA analysis showed that the levels of fibrinolytic and plasmin factors, including thrombin time (TT), prothrombin time (PT), activated partial thromboplastin time (APTT), tissue-type plasminogen activator (t-PA), tissue factor pathway inhibitor (TFPI), and antithrombin III (AT III), were decreased, while those of human fibrinogen (FIB) and D-dimer (D2D) increased significantly in the co-exposure group. Moreover, the myocardial-related enzyme in serum, tested by ELISA, and cardiovascular-related protein expression of atrial natriuretic peptide and brain natriuretic peptide, tested by Western blot assay, was increased in the heart. Furthermore, the expression of inflammation factors such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) was increased in heart tissue subjected to combined exposure, which was manifested by Western blot assay, while the protein levels of angiotensin II (ANG II) and endothelin 1 were (ET-1) elevated in blood vessels in the co-exposure group.ConclusionIn conclusion, the major interactions involved in subacute toxicity due to co-exposure to low doses of SiNPs and Pb on cardiovascular system were expected to be additive and synergistic in nature. Co-exposure to SiNPs and Pb could aggravate the cardiovascular toxicity via endothelial damage, hypercoagulation, and cardiac injury in vivo.

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“…Following the adherence of cells, various concentrations (0, 0.05, 0.125, 0.25, 0.5, 1.0 mg/ml) of MXF were added to culture media for 24 h, 48 h, and 72 h respectively. After the appropriate incubation, 10 uL of CCK-8 solution was added to each cultured well, and the absorbance was measured at 450 nm after a two-hour incubation of HCECs with the reagent 37 .…”

Section: Methodsmentioning

confidence: 99%

Evaluation of moxifloxacin-induced cytotoxicity on human corneal endothelial cells

Park

Kim

Chuck

et al. 2021

Sci Rep

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Moxifloxacin hydrochloride (MXF) is widely used for the prevention of bacterial endophthalmitis after intraocular surgeries. However, the safety issue of intracameral injection of MXF for human corneal endothelial cells (HCECs) is still debatable. In this study, we investigated concentration-dependent cytotoxicity (0.05–1 mg/ml) of MXF for immortalized HCECs (B4G12 cell) and the underlying mechanism. Reactive oxygen generation (ROS) and cell viability after MXF exposure was measured. Flow cytometric analysis and TUNEL assay was used to detect apoptotic HCECs after MXF exposure. Ultrastructure of damaged HCECs by MXF was imaged by transmission electron microscope. Western blot analysis and caspase 2, 3 and 8 analysis were used to reveal the underlying mechanism of MXF induced damage in HCECs. We found that MXF induced dose-dependent cytotoxicity in HCECs. MXF exposure increased ROS generation and induced autophagy in HCECs. Increased LDH release represented the cellular membrane damage by MXF. In addition, caspases activation, Bax/Bcl-xL-dependent apoptosis pathway and apoptosis inducing factor nuclear translocation were all involved in MXF induced HCECs’ damage, especially after exposure to high dose of MXF (0.5 and 1.0 mg/ml). These findings suggest that MXF toxicity on HCECs should be thoroughly considered by ophthalmologists when intracameral injection of MXF is planned.

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Safety of Nonporous Silica Nanoparticles in Human Corneal Endothelial Cells

Cited by 29 publications

References 49 publications

Targeting autophagy using metallic nanoparticles: a promising strategy for cancer treatment

Targeting autophagy using metallic nanoparticles: a promising strategy for cancer treatment

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Evaluation of moxifloxacin-induced cytotoxicity on human corneal endothelial cells

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