Triphenyl phosphate exposure induces kidney structural damage and gut microbiota disorders in mice under different diets

Cui, Haiyan; Chang, Yeqian; Jiang, Xiaofeng; Li, Mei

doi:10.1016/j.envint.2020.106054

Cited by 22 publications

(7 citation statements)

References 53 publications

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“…Actually, it was verified that exposure to mixed OPEs was positively related to the increased prevalence of cardiovascular disease among US adults . Consistent with the above phenomenon, triphenyl phosphate (TPHP) exposure led to significant increases in the concentrations of TG and CHO in mice kidney . Moreover, TPHP and tricresyl phosphate (TCrP) treatment also resulted in TG and CHO deposition in human hepatocellular cells, which further supported our finding of lipid accumulation induced by OPEs.…”

Section: Resultssupporting

confidence: 78%

Lipid Metabolic Disorders Induced by Organophosphate Esters in Silver Carp from the Middle Reaches of the Yangtze River

Liu,

Zhang,

et al. 2024

Environ. Sci. Technol.

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The Yangtze River fishery resources have declined strongly over the past few decades. One suspected reason for the decline in fishery productivity, including silver carp (Hypophthalmichthys molitrix), has been linked to organophosphate esters (OPEs) contaminant exposure. In this study, the adverse effect of OPEs on lipid metabolism in silver carp captured from the Yangtze River was examined, and our results indicated that muscle concentrations of the OPEs were positively associated with serum cholesterol and total lipid levels. In vivo laboratory results revealed that exposure to environmental concentrations of OPEs significantly increased the concentrations of triglyceride, cholesterol, and total lipid levels. Lipidome analysis further confirmed the lipid metabolism dysfunction induced by OPEs, and glycerophospholipids and sphingolipids were the most affected lipids. Hepatic transcriptomic analysis found that OPEs caused significant alterations in the transcription of genes involved in lipid metabolism. Pathways associated with lipid homeostasis, including the peroxisome proliferator-activated receptor (PPAR) signal pathway, cholesterol metabolism, fatty acid biosynthesis, and steroid biosynthesis, were significantly changed. Furthermore, the affinities of OPEs were different, but the 11 OPEs tested could bind with PPARγ, suggesting that OPEs could disrupt lipid metabolism by interacting with PPARγ. Overall, this study highlighted the harmful effects of OPEs on wild fish and provided mechanistic insights into OPE-induced metabolic disorders.

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Section: Resultssupporting

confidence: 78%

Lipid Metabolic Disorders Induced by Organophosphate Esters in Silver Carp from the Middle Reaches of the Yangtze River

Liu,

Zhang,

et al. 2024

Environ. Sci. Technol.

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“…Whereas caspase-3 promotes GSDME pore formation during apoptosis 35 . Recently, more and more studies have shown that caspase-3 is highly related to the activation of in ammasome and GSDME-induced pyroptosis [36][37][38] . Although the speci c relationship between caspase-3 and the NLRP3 in ammasome has not been clearly reported.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: ELP2 -NLRP3-GSDMD/GSDME mediated pyroptosis induced by TNF-α during osteogenic differentiation

Xia²,

et al. 2022

Preprint

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Elongated protein 2 (ELP2) affects inflammatory responses through the JAK-STAT3 cascade and downstream pathways which regulates ontogenesis. Our recent experiment suggests that TNF-a induced inflammation during ontogenesis is inextricably linked to pyroptosis and is critical for inhibiting osteogenic differentiation. However, we do not know the effect of ELP2 on pyroptosis under inflammatory microenvironment. Thus, this study aims to investigate the role of ELP2 in molecular mechanism for MC3T3-E1 cell pyroptosis. Firstly, using scanning electron microscope, we observed MC3T3-E1 cells underwent obvious cell membrane rupture and inflammation after 48h of TNF-α treatment under ontogenesis induction. Then, we targeted ELP2 associated with the NLRP3 inflammasome identified by bioinformatics analysis. Besides, the effect of ELP2 on the inflammasome was determined by the detection of STAT3/NLRP3/ASC protein in ELP2 knockdown and overexpression cells. The interaction between ELP2 and NLRP3 was confirm by co-immunoprecipitation. Pyroptosis downstream was demonstrated by activation of Caspase-1 and Caspase-3, cleavage of downstream gas protein D (GSDMD) and gas protein E (GSDME/DFNA5). Clarifying the effect of ELP2 on the degree of apoptosis by Fluorescent Staining and Flow Quantitative Analysis of Cell Death Staining. Finally, the effects of ELP2 on ontogenesis was evaluated by detecting the osteogenic associated protein OPN/OCN/RUNX2/ALP expression using western blot and qPCR, also we conducted the ALP staining after the cell was stimulated with TNF-α. From the data in this study, we get ELP2-NLRP3-GSDMD/GSDME mediated pyroptosis induced by TNF-α during osteogenic differentiation. Regulation of ELP2 may be a potential target for the treatment of bone infections.

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“…Notably, ELP2 overexpression can cause MC3T3‐E1 pyroptosis via the classical NLRP3 inflammasome pathway since it activates NLRP3, ASC, and caspase‐1 after 24 h of TNF‐α exposure, and causes caspase‐1 protein cleavage 34,35 . Caspase‐3 promotes GSDME pore formation during apoptosis 36 and an increasing number of studies have suggested that caspase‐3 is highly related to NLRP3 inflammasome activation and GSDME‐induced pyroptosis 37,38 . Although the specific relationship between caspase‐3 and the NLRP3 inflammasome has not yet been elucidated, our findings suggest an association between these proteins.…”

Section: Discussionmentioning

confidence: 99%

ELP2‐NLRP3‐GSDMD/GSDME‐mediated pyroptosis is induced by TNF‐α in MC3T3‐E1 cells during osteogenic differentiation

Xia,

Ou,

Yang

et al. 2023

J Cellular Molecular Medi

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Tumour necrosis factor‐α (TNF‐α) is a cytokine involved in systemic inflammation. TNF‐α slows down osteogenic differentiation, which may contribute to poor bone development in the inflammatory microenvironment. TNF‐α inhibits osteogenic differentiation by activating the JAK‐STAT3 pathway, of which Signal transducer and activator of transcription 3 (STAT3)‐interacting protein 1 (StIP1, also known as elongator complex protein 2, ELP2) is a key protein in the JAK‐STAT3 pathway. We investigated whether and how ELP2 activation mediates the TNF‐α‐induced pyroptosis during osteoblastic differentiation. Using in vitro cell cultures of preosteoblastic MC3T3‐E1 cells, we found that TNF‐α exposure causes cell pyroptosis in an inflammatory microenvironment during osteoblastic differentiation. Bioinformatics, protein docking model and co‐immunoprecipitation analysis revealed an association between ELP2, STAT3 and NLRP3. Forced ELP2 expression promoted MC3T3‐E1 cells pyroptosis, with an increase in the expression of STAT3, NLRP3 inflammasome, GSDMD/GSDME, osteoblast marker genes, and the activity of alkaline phosphatase. In contrast, ELP2 silencing ameliorated MC3T3‐E1 cells pyroptosis, and osteogenic differentiation, especially after TNF‐α stimulation. The TNF‐α‐induced cells pyroptosis during osteoblastic differentiation was therefore mediated by ELP2. These results suggest that ELP2 is upregulated at the pyroptosis of MC3T3‐E1 cells and inhibits osteogenic differentiation in response to TNF‐α through NLRP3‐GSDMD/GSDME activation.

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Triphenyl phosphate exposure induces kidney structural damage and gut microbiota disorders in mice under different diets

Cited by 22 publications

References 53 publications

Lipid Metabolic Disorders Induced by Organophosphate Esters in Silver Carp from the Middle Reaches of the Yangtze River

Lipid Metabolic Disorders Induced by Organophosphate Esters in Silver Carp from the Middle Reaches of the Yangtze River

WITHDRAWN: ELP2 -NLRP3-GSDMD/GSDME mediated pyroptosis induced by TNF-α during osteogenic differentiation

ELP2‐NLRP3‐GSDMD/GSDME‐mediated pyroptosis is induced by TNF‐α in MC3T3‐E1 cells during osteogenic differentiation

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