Silica-Induced TNF-<i>α</i>and TGF-<i>β</i>1 Expression in RAW264.7 Cells are Dependent on Src-ERK/AP-1 Pathways

Li, Xiang; Hu, Yongbin; Jin, Zhongyuan; Hai-ying, Jiang; Wen, Ji

doi:10.1080/15376510802354201

Cited by 24 publications

(14 citation statements)

References 31 publications

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“…In our study, the level of TNF‐α in the supernatant of SiO 2 ‐stimulated RAW264.7 cells increased with increasing time and was reduced after MT treatment. TNF‐α might induce autophagy in a Src‐ERK/AP1 pathway‐dependent manner , which is one of the three MAPK ERK families involved in cell proliferation and differentiation induced by AP1 . This result was consistent with a previous report .…”

Section: Discussionsupporting

confidence: 93%

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

Zhang

et al. 2019

IUBMB Life

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Melatonin is one of the main hormones that regulate biological rhythms and have immunomodulation, anti‐inflammatory, and antioxidation functions. In this study, we aimed to explore the effect of melatonin on the autophagy, apoptosis, and inflammatory reaction of macrophages (RAW264.7 cells) stimulated by nanosilica. SiO2 (100 mg/mL, 10–20 nm) was used to stimulate RAW264.7 cells at different time points (0, 2, 4, 8, 12, and 24 hr). Melatonin (200 μM) was added to SiO2‐stimulated macrophages at 12 hr. Beclin‐1, LC3, Bax, Bcl‐2, and Caspase‐3 were examined with western blotting. Flow cytometry was used to detect apoptosis. The levels of TNF‐α, IL‐1β, and IL‐18 were detected by ELISA. The level of TNF‐α in the supernatant of SiO2‐stimulated cells gradually increased with time but decreased following melatonin administration. In contrast, the expression of IL‐1β and IL‐18 increased after melatonin treatment. LC3 and Bax signaling pathways were activated in SiO2‐stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin‐treated cells. GFP‐LC3 puncta were significantly increased in SiO2‐stimulated RAW264.7 cells and decreased in melatonin‐treated cells. The apoptotic rate in SiO2‐stimulated RAW264.7 cells increased with time and decreased after melatonin treatment, and the number of phagosomes increased with the stimulation of nanosilica and the treatment of melatonin. Melatonin might promote autophagy and inhibit apoptosis as well as inflammatory responses of RAW264.7 cells stimulated by nanosilica. © 2019 IUBMB Life, 2019

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Section: Discussionsupporting

confidence: 93%

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

Zhang

et al. 2019

IUBMB Life

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“…Meanwhile, TNF‐α is considered a central mediator of chronic inflammatory diseases. It has been reported that both TGF‐β1 and TNF‐α can be stimulated by inflammatory stimuli in macrophages 38, 39. Therefore, we next detected the production of TGF‐β1 and TNF‐α from MWCNT‐stimulated macrophages.…”

Section: Resultsmentioning

confidence: 96%

Multiwall Carbon Nanotubes Mediate Macrophage Activation and Promote Pulmonary Fibrosis Through TGF‐β/Smad Signaling Pathway

Wang

Nie

Wang

et al. 2013

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Multiwall carbon nanotubes (MWCNTs) have been widely used in many disciplines due to their unique physical and chemical properties, but have also raised great concerns about their possible negative health impacts, especially through occupational exposure. Although recent studies have demonstrated that MWCNTs induce granuloma formation and/or fibrotic responses in the lungs of rats or mice, their cellular and molecular mechanisms remain largely unaddressed. Here, it is reported that the TGF-β/Smad signaling pathway can be activated by MWCNTs and play a critical role in MWCNT-induced pulmonary fibrosis. Firstly, in vivo data show that spontaneously hypertensive (SH) rats administered long MWCNTs (20-50 μm) but not short MWCNTs (0.5-2 μm) exhibit increased fibroblast proliferation, collagen deposition and granuloma formation in lung tissue. Secondly, the in vivo experiments also indicate that only long MWCNTs can significantly activate macrophages and increase the production of transforming growth factor (TGF)-β1, which induces the phosphorylation of Smad2 and then the expression of collagen I/III and extracellular matrix (ECM) protease inhibitors in lung tissues. Finally, the present in vitro studies further demonstrate that the TGF-β/Smad signaling pathway is indeed necessary for the expression of collagen III in fibroblast cells. Together, these data demonstrate that MWCNTs stimulate pulmonary fibrotic responses such as fibroblast proliferation and collagen deposition in a TGF-β/Smad-dependent manner. These observations also suggest that tube length acts as an important factor in MWCNT-induced macrophage activation and subsequent TGF-β1 secretion. These in vivo and in vitro studies further highlight the potential adverse health effects that may occur following MWCNT exposure and provide a better understanding of the cellular and molecular mechanisms by which MWCNTs induce pulmonary fibrotic reactions.

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“…We observed that ROS formation in these cells was slightly lower than that in RLE-6TN cells after exposure to four of the six NMs with ROS inducing potential (Figures 2,3,4,5,6,7). The murine peritoneal macrophage cell line RAW264.7 displays similarities with alveolar macrophages [42] and has been widely used in studies investigating the pulmonary toxic potential of particulate matter [e.g. [43,44] and NMs [e.g.…”

Section: Resultsmentioning

confidence: 99%

Cytotoxicity screening of 23 engineered nanomaterials using a test matrix of ten cell lines and three different assays

et al. 2011

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BackgroundEngineered nanomaterials display unique properties that may have impact on human health, and thus require a reliable evaluation of their potential toxicity. Here, we performed a standardized in vitro screening of 23 engineered nanomaterials. We thoroughly characterized the physicochemical properties of the nanomaterials and adapted three classical in vitro toxicity assays to eliminate nanomaterial interference. Nanomaterial toxicity was assessed in ten representative cell lines.ResultsSix nanomaterials induced oxidative cell stress while only a single nanomaterial reduced cellular metabolic activity and none of the particles affected cell viability. Results from heterogeneous and chemically identical particles suggested that surface chemistry, surface coating and chemical composition are likely determinants of nanomaterial toxicity. Individual cell lines differed significantly in their response, dependent on the particle type and the toxicity endpoint measured.ConclusionIn vitro toxicity of the analyzed engineered nanomaterials cannot be attributed to a defined physicochemical property. Therefore, the accurate identification of nanomaterial cytotoxicity requires a matrix based on a set of sensitive cell lines and in vitro assays measuring different cytotoxicity endpoints.

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Silica-Induced TNF-αand TGF-β1 Expression in RAW264.7 Cells are Dependent on Src-ERK/AP-1 Pathways

Cited by 24 publications

References 31 publications

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

Multiwall Carbon Nanotubes Mediate Macrophage Activation and Promote Pulmonary Fibrosis Through TGF‐β/Smad Signaling Pathway

Cytotoxicity screening of 23 engineered nanomaterials using a test matrix of ten cell lines and three different assays

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