Long-term respiratory exposure to amorphous silica nanoparticles promoted systemic inflammation and progression of fibrosis in a susceptible mouse model

Li, Xueyan; Li, Yan; Lv, Songqing; Xu, Hailin; Ma, Ru; Sun, Zhiwei; Li, Yanbo; Guo, Caixia

doi:10.1016/j.chemosphere.2022.134633

Cited by 30 publications

(6 citation statements)

References 81 publications

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“…Both in vivo and in vitro studies have shown that exposure to SiNPs can cause signi cant damage to the lungs. [6,8,30,31] Previous studies have indicated that SiNPs exposure induces pleural and pericardial effusion, pulmonary brosis, and granuloma in rats, which is similar to the symptoms observed in exposed workers. [9,10,32] However, the underlying pathological mechanism of SiNPs remains unknown.…”

Section: Discussionmentioning

confidence: 67%

Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling

Pan

Chang

et al. 2023

Toxicology

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Section: Discussionmentioning

confidence: 67%

Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling

Pan

Chang

et al. 2023

Toxicology

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“…Considering the applicability and accessibility of SiNPs, the toxicity of SiNPs should be exactly estimated. A large number of studies have confirmed that SiNPs could enhance lung permeability, exacerbate pulmonary inflammation and fibrosis progression, , and even present the carcinogenic potential of lung cancer . Likewise, we noticed lung interstitial injury in rat lung tissues exposed to SiNPs, as manifested by alveolar septa thickening (Figure A) and collagen hyperplasia (Figure B–C).…”

Section: Discussionmentioning

confidence: 99%

Lung Single-Cell Transcriptomics Offers Insights into the Pulmonary Interstitial Toxicity Caused by Silica Nanoparticles

Li,

Yao,

et al. 2024

Environ. Health

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The adverse respiratory outcomes motivated by silica nanoparticles (SiNPs) exposure have received increasing attention. Herein, we aim to elucidate the interplay of diverse cell populations in the lungs and key contributors in triggering lung injuries caused by SiNPs. We conducted a subchronic respiratory exposure model of SiNPs via intratracheal instillation in Wistar rats, where rats were administered with 1.5, 3.0, or 6.0 mg/kg body weight SiNPs once a week for 12 times in total. We revealed that SiNPs caused pulmonary interstitial injury in rats by histopathological examination and pulmonary hydroxyproline determination. Further, a single-cell RNA-Seq via screening 10 457 cells in the rat lungs disclosed cell-specific responses to SiNPs and cell-to-cell interactions within the alveolar macrophages, epithelial cells, and fibroblasts from rat lungs. These disturbed responses were principally related to the dysregulation of protein homeostasis (proteostasis), accompanied by an inflammatory response in macrophages, cell death in epithelial, proliferation, and extracellular matrix deposition in fibroblast. These cell-specific responses may serve a synergistic role in the pathogenesis of pulmonary interstitial disease triggered by SiNPs. In particular, the analyses of gene interaction networks and gene−disease associations filtered out heat shock proteins (Hsps) family genes crucial to the observed pulmonary lesions caused by SiNPs. Of note, both GEO database analysis and our experiments' validation indicated that Hsps, especially Hspd1, may be a key contributor to pulmonary interstitial injury, possibly through triggering oxidative stress, immune response, and disrupting protein homeostasis. Taken together, our study provides insights into pulmonary toxic effects and underlying molecular mechanisms of SiNPs from a single-cell perspective.

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“…Liver is commonly regarded as a major organ for deposition of NPs after absorption. Previous studies have revealed SiNPs exposure could cause inflammation, liver injury and even hepatic fibrosis [ 7 , 39 , 40 ], hinting its possible role on the development of MAFLD. Indeed, our data revealed SiNPs exposure facilitated the progression of MAFLD using in vivo and in vitro investigations.…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that inhaled particles could be detected in extrapulmonary organs [ 4 , 5 ]. To date, numerous studies have revealed that SiNPs exposure led to harmful biological responses in diverse organs [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…A number of toxicological studies have indicated that SiNPs caused liver injury, including oxidative stress, DNA damage, inflammation, disturbance in metabolism [ [10] , [11] , [12] ], etc., probably contributing fibrosis and liver failure ultimately [ [13] , [14] , [15] ]. Currently, the nano-safety of susceptible populations is of great concern [ 7 , 16 ]. However, the interactions between SiNPs and biological systems under disease-state condition, and underlying mechanisms are poorly elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Silica nanoparticles aggravated the metabolic associated fatty liver disease through disturbed amino acid and lipid metabolisms-mediated oxidative stress

Abulikemu

Zhao

et al. 2023

Redox Biology

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Long-term respiratory exposure to amorphous silica nanoparticles promoted systemic inflammation and progression of fibrosis in a susceptible mouse model

Cited by 30 publications

References 81 publications

Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling

Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling

Lung Single-Cell Transcriptomics Offers Insights into the Pulmonary Interstitial Toxicity Caused by Silica Nanoparticles

Silica nanoparticles aggravated the metabolic associated fatty liver disease through disturbed amino acid and lipid metabolisms-mediated oxidative stress

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