Effects of abnormal expression of fusion and fission genes on the morphology and function of lung macrophage mitochondria in SiO2-induced silicosis fibrosis in rats in vivo

Zhao-qiang, Zhang; Zhang, Chunzhi; Daohua, Pang; Han, Gui-zhi; Lin, Li

doi:10.1016/j.toxlet.2019.04.029

Cited by 17 publications

(20 citation statements)

References 38 publications

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“…First, the effects of exposure to different concentrations of PM 2.5 on HBE and HUVEC cells was evaluated. The results indicated that PM 2.5 exposure significantly reduced cell viability in a dose-dependent manner, enhanced the lipid oxidation index of Mda and decreased the anti-oxidative stress index of Sod, which was in line with previously published reports (27,28). Moreover, PM 2.5 addition to cell culture media significantly increased the accumulation of pro-inflammatory factors IL-1β, il-6 and TnF-α, inhibited the production of inflammatory factor il-2, activated the inflammatory response and promoted lung injury and fibrosis.…”

Section: Discussionsupporting

confidence: 92%

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

et al. 2020

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There have been few studies investigating the potential effects of indoor sources of particulate matter on human health. in this study, the effect of different concentrations of fine particulate matter (PM 2.5) collected from a printing room on lung health was examined using cultured cells and a mouse model. Further, the mechanism of lung injury was examined. The results indicated that PM 2.5 significantly enhanced malondialdehyde activity (P<0.05), decreased superoxide dismutase activity (P<0.05), upregulated the expression of pro-inflammatory factors including interleukin (IL)-1β, tumor necrosis factor-, il-6 and downregulated the expression of the inflammatory factor IL-2 (P<0.05). Western blot analysis indicated that PM 2.5 significantly enhanced expression of phosphorylated (p)-ERK relative to total ERK, cyclooxygenase-2, p-anti-nuclear-factor-κB (p-NF-κB) relative to nF-κB, transforming growth factor-β1 and Bax relative to Bcl-2 in inflammation (P<0.05), fibrosis and apoptosis signaling pathways. Furthermore, the results revealed that exposure was associated with an increased abundance of pathogens including Burkholderiales, Coriobacteriia, and Betaproteobacteria in in the lungs. in conclusion, exposure to PM 2.5 from a printing room significantly increased inflammation, fibrosis, apoptosis and the abundance of pathogenic bacteria, indicating that exposure is potential threat to individuals who spend a significant amount of time in printing rooms.

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Section: Discussionsupporting

confidence: 92%

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

et al. 2020

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“…Workers who cut, polish or grindstone materials can be exposed to silica dust 4 . Pulmonary fibrosis is characterized by a persistent inflammatory and subsequent fibroblast proliferation and activation, abnormal collagen deposition 5‐7 . However, there are no specific therapies for pulmonary fibrosis, and little is known about its precise molecular mechanism.…”

Section: Introductionmentioning

confidence: 99%

Silica dust exposure induces pulmonary fibrosis through autophagy signaling

Shi

Wang³

et al. 2021

Environmental Toxicology

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Silicosis is a well‐acknowledged occupational lung disease caused by inhalation of a large amount of free silica dust during the production period and eventually a considerable negative impact on the patients' quality of life. Autophagy exerts a critical influence on immune and inflammatory responses during the pathogenesis of pulmonary fibrosis. In this study, we sought to determine whether autophagy is involved in silicosis's pathogenesis and how it may affect pulmonary cellular physiology. In the animal experiments, we found persistent activation of autophagy in the development of pulmonary fibrosis, which was also accompanied by tumor necrosis factor and transforming growth factor expression increased. Therefore, the autophagy signaling pathway may regulate the inflammatory response and affect the progression of fibrosis. Further, in vitro experiments, we used LY294002, RAPA, and N‐acetylcysteine (NAC) intervened autophagy. Our results showed that PI3K/Akt/mTOR signaling pathway is involved in the autophagy changed mediated by SiO2 exposed, and autophagy might play a protective role in the progression of pulmonary fibrosis. Additionally, NAC's effect is not apparent on SiO2‐mediated autophagy through the PI3K/Akt/mTOR signaling pathway, but it can reduce the inflammatory response on NR8383 cells mediated by SiO2‐exposed. Nevertheless, it's interesting that NAC can reduce the inflammatory response on NR8383 cells mediated by SiO2‐exposed. Taken together, our data demonstrated that SiO2‐exposed can induce pulmonary fibrosis along with autophagy both in vivo and in vitro, NAC could alleviate the inflammatory response NR8383 cells by SiO2‐exposed through non PI3K/Akt/mTOR signaling pathway, and the specific mechanism of its action needs further studying.

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“…Subsequently, Parkin ubiquitinates and degrades MFN1/2, and connects to LC3B II through adaptor protein SQSTM1/p62, which leads to autophagosome formation and mitophagy [31]. The process of mitophagy removes damaged mitochondria to maintain a healthy mitochondrial pool, but an excessive rate of mitophagy may induce the reduction of mitochondrial quantity, the inhibition of mitochondrial respiratory function and bioenergy production, and the increase of mtROS levels [32].…”

Section: Discussionmentioning

confidence: 99%

Chronic lung inflammation and pulmonary fibrosis after multiple intranasal instillation of PM2.5 in mice

Zhang

et al. 2020

Preprint

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Background: Fine particulate matter (PM 2.5 ) is an important component of air pollution and can induce lung inflammation and oxidative stress. We hypothesised that PM 2.5 could play a role in the induction of pulmonary fibrosis. We examined whether multiple intranasal instillation of PM 2.5 can induce pulmonary fibrosis in the mouse, and also investigated the underlying pro-fibrotic signaling pathways.Methods: C57/BL6 mice were intranasally instilled with 50 μl of PM 2.5 suspension (7.8 μg/g body weight) or PBS three times a week over 3 weeks, 6 weeks or 9 weeks. To observe the recovery of pulmonary fibrosis after the termination of PM 2.5 exposure, 9 week-PM 2.5 instilled mice were also studied at 3 weeks after termination of instillation.Results: There were significant decreases in total lung capacity (TLC) and compliance (Cchord) in the 9-week PM 2.5 -instilled mice, while there was an increase in total cell counts in bronchoalveolar fluid and lung section in 3-week, 6-week and 9-week PM 2.5 -instilled mice and 9 week-PM 2.5 instilled-3 week-air exposed mice. There were increased histological fibrosis scores with enhanced type I collagen and hydroxyproline deposition in lung tissue in 6-week and 9-week PM 2.5 -instilled mice and 9-week-PM 2.5 instilled-3-week-air-exposed mice. Multiple PM 2.5 instillation resulted in increased expression of TGFβ1, increases of N-Cadherin and Vimentin and decrease of E-Cadherin. It also led to decreases in OPA1 and MFN2, and increases in Parkin, SQSTM1/p62, the ratio of light china (LC) 3B II to LC3B I, PI3k/Akt phosphorylation, NOX4 and NLRP3 expression.Conclusions: The intranasal instillation of PM 2.5 for 9 weeks induced lung inflammation and pulmonary fibrosis, which was linked with aberrant epithelial-mesenchymal transition, mitochondrial damage and mitophagy, as well as activation of TGFβ1-PI3K/Akt and TGFβ1-NOX4 -NLRP3 pathways.

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Effects of abnormal expression of fusion and fission genes on the morphology and function of lung macrophage mitochondria in SiO2-induced silicosis fibrosis in rats in vivo

Cited by 17 publications

References 38 publications

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

Silica dust exposure induces pulmonary fibrosis through autophagy signaling

Chronic lung inflammation and pulmonary fibrosis after multiple intranasal instillation of PM2.5 in mice

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