miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

Shen, Yujie; Zhou, Min; Yan, Junkai; Gong, Zizhen; Xiao, Yongtao; Zhang, Cong; Du, Peng; Chen, Yingwei

doi:10.1152/ajpgi.00316.2016

Cited by 54 publications

(47 citation statements)

References 38 publications

(53 reference statements)

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“…The tight junction proteins mainly include claudin-5, occludin and ZO-1 [23]. It has been reported inflammation plays a key role in tight junction disruption and many inflammation factors can modulate the expression of tight junction proteins [24]. For example, TNF-α was shown to decrease occludin expression in glomerular endothelial cells of mice [25].…”

Section: Discussionmentioning

confidence: 99%

Propofol attenuated TNF-α-modulated occludin expression by inhibiting Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway in hCMEC/D3 cells

et al. 2019

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Background: The levels of tight junction proteins (TJs), especially occludin, correlate with blood-brain barrier (BBB) disruption caused by inflammation in central nervous system (CNS). It has been reported that propofol, the most commonly used anesthetic, could inhibit inflammation response in CNS. In this study, we investigated the effects of tumor necrosis factor-α (TNF-α) and propofol on occludin expression in human cerebral microvascular endothelial cell line, D3 clone (hCMEC/D3 cells), and explored the underlying mechanisms. Methods: The hCMEC/D3 cells were treated with propofol, followed by TNF-α. The expression and phosphorylation of Hif-1α, VEGF, VEGFR-2, ERK, p38MAPK and occludin were measured by Western blot analysis. The cell viability of hCMEC/D3 cells was measured by cell counting kit-8. Results: TNF-α (10 ng/ml, 4 h) significantly decreased the expression of occludin, which was attenuated by propofol (25 μM). TNF-α induced Hif-1α/VEGF/VEGFR-2/ERK signaling pathway, while propofol could inhibit it. TNF-α induced the phosphorylation of p38MAPK, while propofol had no effect on it. In addition, the inhibitors of Hif-1α, VEGFR-2, and ERK could reduce the effect of TNF-α on occludin expression. Conclusion: TNF-α could decrease the expression of occludin via activating Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway, which was attenuated by propofol.

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Section: Discussionmentioning

confidence: 99%

Propofol attenuated TNF-α-modulated occludin expression by inhibiting Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway in hCMEC/D3 cells

et al. 2019

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“…Recent evidence has shown that miRNAs play a vital role in controlling intestinal epithelial barrier function, in part by regulating the expression of tight junction proteins (Martinez et al, 2017). MiR-200c is a member of the miR-200 family, in which miR-200b and miR-429 have been shown to be involved in the regulation of intestinal epithelial barrier function (Yu et al, 2016;Shen et al, 2017). Many reports revealed that miR-200c plays a key role in the epithelial-mesenchymal transition, apoptosis, proliferation, and metastasis of various cancer cells (Mutlu et al, 2016;.…”

Section: Introductionmentioning

confidence: 99%

“…Among them, it has been reported that miR-429 can down-regulate the expression of Ocln by targeting the 3′-UTR of Ocln mRNA, leading to the destruction of tight junction and enhanced intestinal barrier permeability (Yu et al, 2016). In addition, miR-200b has been demonstrated to attenuate tight junction injury induced by tumor necrosis factor a through targeting c-Jun and MLCK (Shen et al, 2017). We found that FA significantly inhibited the decreased expression of miR-200c-3p induced by LPS.…”

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confidence: 99%

Ferulic Acid Ameliorates Lipopolysaccharide-Induced Barrier Dysfunction via MicroRNA-200c-3p-Mediated Activation of PI3K/AKT Pathway in Caco-2 Cells

Guo

Zhao

et al. 2020

Front. Pharmacol.

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Intestinal barrier dysfunction is an important clinical problem in various acute and chronic pathological conditions. Ferulic acid (FA) can attenuate the intestinal epithelial barrier dysfunction, however, the underlying mechanism remains unclear. The present study aimed to uncover the protective effect of FA on intestinal epithelial barrier dysfunction in a Caco-2 cell model of lipopolysaccharide (LPS) stimulation and the underlying mechanism. Caco-2 cells were pretreated with FA and then exposed to LPS stimulation. The barrier function of Caco-2 cells was evaluated by measuring trans-epithelial resistance (TER) and 4-kDa fluorescein isothiocyanate (FITC)-dextran (FD4) flux, and analyzing the tight junction protein expression and structure. The results showed that decreased TER and increased FITC-FD4 flux were observed in Caco-2 cells stimulated with LPS, but these effects were attenuated by FA pretreatment. FA pretreatment inhibited LPS-induced decrease in occludin and ZO-1 mRNA and protein expression. LPS stimulation decreased miR-200c-3p expression, whereas this decrease was inhibited by FA pretreatment. Furthermore, overexpression of miR-200c-3p strengthened the protective effects of FA on LPS-induced Caco-2 cell barrier dysfunction by decreasing epithelial permeability, increasing occludin and ZO-1 protein expression, and maintaining of ZO-1 protein distribution, while suppression of miR-200c-3p reversed the protective effects of FA. LPS treatment increased the expression of PTEN protein and decreased expression of phosphorylated PI3K and AKT proteins. However, pretreatment of FA inhibited expression of PTEN protein and promoted activation of PI3K/AKT signaling pathway in the LPS-treated Caco-2 cells, and this regulatory effect of FA on the PTEN/PI3K/AKT signaling pathway was strengthened or weakened by miR-200c-3p overexpression or suppression, respectively. Our findings suggested that in Caco-2 cells, FA promotes activation of PI3K/AKT pathway by miR-200c-3p-mediated suppression of the negative

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“…The multiple tight junction proteins includes claudins, occludin and zonula occludens-1 (ZO-1) [18]. It has been reported that the imflammation factors could impact the expression of tight junction proteins [19]. It also has been reported that the levels of imflammation factors were raised due to surgical trauma during perioperative period [20].…”

Section: Discussionmentioning

confidence: 99%

Propofol attenuated the effect of TNF-α on occludin expression by inhibiting HIF-1α/VEGF/VEGFR-2/ERK signaling pathway in hCMEC/D3 cells

Zhang

Ding

Miao

et al. 2019

Preprint

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Purpose The levels of tight junction proteins (TJs), especially occludin correlate with blood-brain barrier (BBB) disruption caused by central nervous system (CNS) inflammation during perioperative period. It has been reported that propofol, the most commonly used anesthetic, could inhibit inflammation response in CNS. In this study, we investigated the effects of TNF-α and propofol on occludin expression in human cerebral microvascular endothelial cell line, D3 clone (hCMEC/D3 cells), and explored the underlying mechanisms. Methods The hCMEC/D3 cells were treated with propofol, followed by TNF-α. The expression and phosphorylation of HIF-1α, VEGF, VEGFR-2, ERK and occludin were measured by Western blot analysis. Results TNF-α (10 ng/ml, 4 h) significantly decreased the expression of occludin, which was attenuated by propofol (25 μM). TNF-α induced HIF-1α/VEGF/VEGFR-2/ERK signaling pathway, while propofol could inhibit it. In addition, the inhibitors of HIF-1α, VEGF, VEGFR-2, and ERK could reduce the effect of TNF-α on occludin expression. Conclusion TNF-α could decrease the expression of occludin via HIF-1α/VEGF/VEGFR-2/ERK signaling pathway, which was attenuated by propofol.

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miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

Cited by 54 publications

References 38 publications

Propofol attenuated TNF-α-modulated occludin expression by inhibiting Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway in hCMEC/D3 cells

Propofol attenuated TNF-α-modulated occludin expression by inhibiting Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway in hCMEC/D3 cells

Ferulic Acid Ameliorates Lipopolysaccharide-Induced Barrier Dysfunction via MicroRNA-200c-3p-Mediated Activation of PI3K/AKT Pathway in Caco-2 Cells

Propofol attenuated the effect of TNF-α on occludin expression by inhibiting HIF-1α/VEGF/VEGFR-2/ERK signaling pathway in hCMEC/D3 cells

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