Paraquat induce pulmonary epithelial–mesenchymal transition through transforming growth factor-β1-dependent mechanism

Xie, Linshen; Zhou, Dingzi; Xiong, Jingyuan; You, Jia; Zeng, Ye; Peng, Lijun

doi:10.1016/j.etp.2015.09.010

Cited by 24 publications

(23 citation statements)

References 46 publications

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“…For example, transforming growth factor β (TGF- β ) is considered to be one of the main cytokines in paraquat-induced pulmonary fibrosis, and it is also a research hotspot of scholars at home and abroad. Paraquat can induce EMT and active TGF- β /Smad signal pathway [ 24 , 25 ]. Our results showed that paraquat can activate EMT by inhibiting E-cadherin mRNA and protein expression of A549 cells and promoting vimentin mRNA and protein expression.…”

Section: Discussionmentioning

confidence: 99%

Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway

Huang¹

2020

Computational and Mathematical Methods in Medicine

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Objective. In recent years, pulmonary fibrosis caused by paraquat poisoning is still concerned. However, no effective drugs have been developed yet to treat paraquat-induced pulmonary fibrosis. The aim of our research is to investigate whether imrecoxib can inhibit paraquat-induced pulmonary fibrosis and its possible mechanism. Methods. Extraction of primary pulmonary fibrosis cells (PPF cells) in vitro by the method of trypsin digestion. RT-qPCR and western blot were employed to measure the transcription level and protein expression of EMT related markers in paraquat-induced A549 cells. MTT, wound-healing, and Transwell experiments were used to verify the effect of imrecoxib on the proliferation, migration, and invasion of PPF and HFL1 cells. Results. Firstly, our results confirmed that paraquat can induce EMT and activate the NF-κB/snail signal pathway in lung epithelial cell A549. Furthermore, experimental results showed that imrecoxib could repress the proliferation, migration, and invasion of PPF and HFL1 cells. Finally, our study found that imrecoxib can inhibit EMT of paraquat-induced A549 cells by the NF-κB/snail signal pathway. Conclusion. Imrecoxib can inhibit EMT of paraquat-induced A549 cells and alleviate paraquat-caused pulmonary fibrosis through the NF-κB/snail signal pathway. Therefore, imrecoxib is a drug worthy of study in the treatment of paraquat-induced pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway

Huang¹

2020

Computational and Mathematical Methods in Medicine

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“…Previous study has indicated that TGF‐β1 levels in serum and pulmonary tissue increased in rats treated with PQ (Kan et al, ). The TGF‐β/Smad signaling was activated by PQ as evidenced by increased expression of TGF‐β1 and phosphorylation of Smad2/3, inhibiting the expressions of phospho‐Smad2 and phospho‐Smad3 attenuated PQ‐induced EMT as well as fibronectin secretion (Han et al, ; Xie et al, ). In the present study, we investigated the effect of the exogenous H 2 S donor on PQ‐induced EMT.…”

Section: Introductionmentioning

confidence: 99%

“…The epithelial cells reprogrammed into mesenchymal cells, epithelialmesenchymal transition (EMT), which are involved in embryonic development, wound healing, cancer metastasis and tissue fibrosis (Nieto, Huang, Jackson, & Thiery, 2016). Recently, several studies have indicated the process of EMT involved in the pathogenesis of PQ-induced pulmonary fibrosis (Han, Shen, & Chang, 2015;Xie et al, 2016;Yamada, Aki, Unuma, Funakoshi, & Uemura, 2015). Transforming growth factor (TGF)-β1 is a pivotal cytokine of fibrosis and the TGF-β1/Smad signaling plays an important role in EMT (Xu, Lamouille, & Derynck, 2009).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide attenuates paraquat‐induced epithelial‐mesenchymal transition of human alveolar epithelial cells through regulating transforming growth factor‐β1/Smad2/3 signaling pathway

Bai

Yang

et al. 2018

J of Applied Toxicology

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Exogenous H2S donor, sodium hydrosulfide (NaHS), can influence the bleomycin‐induced pulmonary fibrosis by attenuating the epithelial‐mesenchymal transition (EMT) of alveolar epithelial cells, but whether NaHS affects paraquat (PQ)‐induced EMT and the molecular mechanisms remain unclarified. The aim of the present study is to examine the effect of exogenous NaHS on PQ‐induced EMT in human alveolar epithelial cells (A549 cells) and assess if this effect occurs through regulating transforming growth factor (TGF)‐β1/Smad2/3 signaling pathway. The expressions of endogenous H2S producing enzymes, namely cystathionine β‐synthase, cystathionine γ‐lyase and 3‐mercaptopyruvate sulfur transferase, were detected by reverse transcription‐polymerase chain reaction and western blotting. The induced EMT was assessed by morphological and phenotypic characterizations, and the protein level of E‐cadherin and vimentin were detected by western blotting. To investigate the effect of NaHS on PQ‐induced EMT and potential mechanism, A549 cells were pretreated with NaHS before incubating with PQ and then evaluated by morphological changes, cell migration ability, the expression of EMT markers and TGF‐β1/Smad2/3 signaling pathway related proteins. PQ significantly downregulated the expression levels of cystathionine β‐synthase and cystathionine γ‐lyase, but not 3‐mercaptopyruvate sulfur transferase, in a time‐dependent manner in A549 cells. Exogenous NaHS could significantly retard PQ‐induced morphological changes and cell migration ability. Furthermore, exogenous NaHS significantly upregulated the expression of E‐cadherin, whereas it downregulated the expression of vimentin. In addition, exogenous NaHS could also significantly attenuates PQ‐induced TGF‐β1, phosphorylated Smad2/3 proteins expression, which induced by PQ in a time‐dependent manner. This study provides the first evidence that exogenous NaHS attenuates PQ‐induced EMT and migration of human alveolar epithelial cells through regulating the TGF‐β1/Smad2/3 signaling pathway.

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“…In PF, pulmonary inflammatory cells, pulmonary epithelial cells and mast cells play a direct or indirect role by secreting cytokines, inflammatory mediators and other biologically active substances. 27 Cluster analysis of protein function suggested that many DEPs were associated with damage and defense response and inflammation. In addition, KEGG pathway enrichment revealed that a The KEGG pathway analysis revealed that DEPs were significantly concentrated in the retinol metabolic pathway.…”

Section: Discussionmentioning

confidence: 99%

Comparative Proteomic Analysis of Bleomycin-induced Pulmonary Fibrosis Based on Isobaric Tag for Quantitation

Yang

Jia

et al. 2017

The American Journal of the Medical Sciences

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Paraquat induce pulmonary epithelial–mesenchymal transition through transforming growth factor-β1-dependent mechanism

Cited by 24 publications

References 46 publications

Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway

Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway

Hydrogen sulfide attenuates paraquat‐induced epithelial‐mesenchymal transition of human alveolar epithelial cells through regulating transforming growth factor‐β1/Smad2/3 signaling pathway

Comparative Proteomic Analysis of Bleomycin-induced Pulmonary Fibrosis Based on Isobaric Tag for Quantitation

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