Sodium Propionate Attenuates the Lipopolysaccharide-Induced Epithelial–Mesenchymal Transition via the PI3K/Akt/mTOR Signaling Pathway

Chen, Dan; Qiu, Yu-bao; Gao, Zhiqi; Wu, Yaxian; Wan, Bin-bin; Liu, Gang; Chen, Junliang; Zhou, Qin; Yu, Renqiang; Pang, Qingfeng

doi:10.1021/acs.jafc.0c01302

Cited by 22 publications

(17 citation statements)

References 57 publications

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“…Studies have shown that activation of the PI3K/Akt/mTOR pathway in human umbilical cord mesenchymal stem cell (UC‐MSC)‐derived exosomes exerts antiapoptotic effects on rat cardiomyocytes (H9C2) (Liu et al, 2019). Likewise, sodium propionate suppresses the PI3K/Akt/mTOR signaling pathway attenuating the inflammation induced by LPS (Chen et al, 2020). We found that the BeSO 4 ‐Exos treated RAW 264.7 cells upregulated LDH activity and the inflammatory response, whereas pretreatment with rapamycin alleviated it.…”

Section: Discussionmentioning

confidence: 99%

Serum‐derived exosomes from SD rats induce inflammation in macrophages through the mTOR pathway

Wang

Liu

Sun

et al. 2022

J of Applied Toxicology

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Inhalation of beryllium and its compounds can cause lung injuries, resulting from inflammation and oxidative stress. Multivesicular bodies (MVB), such as exosomes, are membrane vesicles produced by early and late endosomes that mediate intercellular communications. However, the role of exosomes in beryllium toxicity has not been elucidated. This current study aimed to investigate the functional role of exosomes in lung injury resulting from beryllium sulfate (BeSO 4 ). Here, Sprague-Dawley (SD) rats were exposed to 4, 8, and 12 mg/kg BeSO 4 by nonexposed intratracheal instillation. Murine macrophage (RAW 264.7) cells were pretreated with 50 nmol/L rapamycin (an mTOR signaling pathway inhibitor) for 30 min and then cultured for 24 h with 100 μg/mL exosomes, which had been previously isolated from the serum of 12 mg/kg BeSO 4 -treated SD rats. Compared with those of the controls, exposure to BeSO 4 in vivo increased LDH activity, elevated levels of inflammatory cytokines (IL-10, TNF-α, and IFN-γ) alongside inflammation-related proteins expression (COX-2 and iNOS), and enhanced secretion of exosomes from the SD rat's serum. Moreover, the BeSO 4 -Exos-induced upregulation of LDH activity and inflammatory responses in RAW 264.7 cells can be alleviated following pretreatment with rapamycin. Collectively, these results suggest that serum exosomes play an important role in pulmonary inflammation induced by BeSO 4 in RAW 264.7 cells via the mTOR pathway.

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Section: Discussionmentioning

confidence: 99%

Serum‐derived exosomes from SD rats induce inflammation in macrophages through the mTOR pathway

Wang

Liu

Sun

et al. 2022

J of Applied Toxicology

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“…LPS induces airway-centered inflammation and airway fibrosis and remodeling (Takahagi et al, 2020). According to recent studies, LPS induces EMT in BEAS-2B cells and mouse models, which are characterized by a decrease in E-cadherin levels, increased levels of α-SMA, vimentin, MMP2, and MMP9 proteins, and inflammatory response, leading to extracellular matrix deposition and lung fibrosis (Chen et al, 2020). TGF-β1 is a key growth factor involved in inducing inflammatory processes and EMT.…”

Section: Discussionmentioning

confidence: 99%

Effect of Peroxiredoxin 1 on the biological function of airway epithelial cells and epithelial-mesenchymal transition

LIU¹,

SHI²,

WAN³

et al. 2022

Biocell

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Peroxiredoxin 1 (PRDX1) participates in tumor cell proliferation, apoptosis, migration, invasion, and the epithelial-to-mesenchymal transition (EMT). This study aimed to investigate the effect of PRDX1 on the EMT of airway epithelial cells stimulated with lipopolysaccharide (LPS) and transforming growth factor-beta 1 (TGF-β1).PRDX1 overexpression significantly increased the proliferation and migration of human bronchial epithelial (BEAS-2B) cells, reduced cell apoptosis (p < 0.01), and induced EMT and collagen deposition by upregulating the expression of the matrix metallopeptidase (MMP)2, MMP9, α-smooth muscle actin (α-SMA), N-cadherin, vimentin and twist proteins and inhibiting E-cadherin expression (p < 0.05). PRDX1 overexpression promoted TGF-β1-mediated inhibition of cell proliferation and migration and significantly enhanced the TGF-β1-induced EMT and collagen synthesis (p < 0.05).Knockdown of PRDX1 inhibited cell proliferation, migration, EMT, and collagen synthesis (p < 0.01), reversed LPS-mediated inhibition of cell proliferation and migration, and significantly suppressed LPS-induced EMT and collagen synthesis (p < 0.01). The result indicating that PRDX1 may be involved in LPS/TGF-1-induced EMT and collagen synthesis in human bronchial epithelial cells.

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“…In this study, a mesenchymal-like transformation was not observed until 7 d after the LPS induction. However, other cells showed significant morphological changes after 24–72 h of LPS treatment [ 25 , 26 ]. This result is related to the levels of inflammatory factors secreted by the mammary epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

NF-κB–Dependent Snail Expression Promotes Epithelial–Mesenchymal Transition in Mastitis

Liu

Zhao

et al. 2021

Animals

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Mastitis is a common and important clinical disease in ruminants. This may be associated with inflammatory fibrosis if not treated promptly. Inflammation-derived fibrosis is usually accompanied by epithelial–mesenchymal transition (EMT) in epithelial cells. However, the precise molecular mechanism underlying mastitis-induced fibrosis remains unclear. Nuclear factor kappa-B (NF-κB) and Snail are key regulators of EMT. In this study, primary goat mammary epithelial cells (GMECs) were treated with 10 μg/mL lipopolysaccharide (LPS) for 14 d to mimic the in vivo mastitis environment. After LPS treatment, the GMECs underwent mesenchymal morphological transformation and expressed mesenchymal cell markers. Snail expression was induced by LPS and was inhibited by suppression of the TLR4/NF-κB signaling pathway. Snail knockdown alleviated LPS-induced EMT and altered the expression of inflammatory cytokines. Finally, we found that the expression of key molecules of the TLR4/NF-κB/Snail signaling pathway was increased in mastitis tissues. These results suggest that Snail plays a vital role in LPS-induced EMT in GMECs and that the mechanism is dependent on the activation of the TLR4/NF-κB signaling pathway.

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Sodium Propionate Attenuates the Lipopolysaccharide-Induced Epithelial–Mesenchymal Transition via the PI3K/Akt/mTOR Signaling Pathway

Cited by 22 publications

References 57 publications

Serum‐derived exosomes from SD rats induce inflammation in macrophages through the mTOR pathway

Serum‐derived exosomes from SD rats induce inflammation in macrophages through the mTOR pathway

Effect of Peroxiredoxin 1 on the biological function of airway epithelial cells and epithelial-mesenchymal transition

NF-κB–Dependent Snail Expression Promotes Epithelial–Mesenchymal Transition in Mastitis

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