MicroRNA-155-enhanced autophagy in human gastric epithelial cell in response to Helicobacter pylori

Wu, Kai; Zhu, Chao-Hui; Yao, Yi; Wang, Xin; Song, Jiugang; Zhai, Junshan

doi:10.4103/1319-3767.173756

Cited by 34 publications

(18 citation statements)

References 19 publications

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“…miR-155 −/− mice fail to control H. pylori infection as a result of impaired pathogen-specific Th1 and Th17 responses and exhibit significantly lower levels of gastric IFN-α and IL-17 production [ 15 ]. Similarly, overexpression of miR-155 by transfection of miR-155 mimics can significantly decrease the survival of intracellular H. Pylori [ 49 ]. Up-regulation of miR-155 can also lead to the expression of TNF-α [ 50 ].…”

Section: H Pylori -Related Gastric Diseasementioning

confidence: 99%

Expression and Function of miR-155 in Diseases of the Gastrointestinal Tract

Wan

Xia

et al. 2016

IJMS

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MicroRNAs (miRNAs) are a type of small noncoding RNA that can regulate the expression of target genes under physiological and pathophysiological conditions. miR-155 is a multifunctional miRNA with inflammation-related and oncogenic roles. In particular, the dysregulation of miR-155 has been strongly implicated in Helicobacter pylori-related gastric disease, inflammatory bowel disease, and colorectal cancer in addition to being involved in molecular changes of important targets and signaling pathways. This review focuses on the expression and function of miR-155 during inflammation and carcinogenesis and its potential use as an effective therapeutic target for certain gastrointestinal diseases.

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Section: H Pylori -Related Gastric Diseasementioning

confidence: 99%

Expression and Function of miR-155 in Diseases of the Gastrointestinal Tract

Wan

Xia

et al. 2016

IJMS

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“…[8] It has also been reported that the expression of miR-155 was increased or decreased in various diseases and was involved in the development of these diseases by regulating autophagy. [17,19,32,33] In view of the aforementioned reports, we next investigated whether miR-155 exerted its effects on cytokine production by DCs via the process of autophagy. To answer this question, an experiment with miR-155 mimic transfection was performed.…”

Section: Discussionmentioning

confidence: 99%

Decreased MicroRNA-155 in Behcet’s disease leads to defective control of autophagy thereby stimulating excessive proinflammatory cytokine production

Liang

Zhou

Feng

et al. 2020

Preprint

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Background: Earlier we reported that the microRNA (miR)-155 expression in dendritic cells (DCs) from Behcet’s disease (BD) patients was decreased and affected cytokine production of DCs. In this study, we investigated the mechanisms whereby miR-155 regulates cytokine production by DCs.Methods: The formation of autophagosomes in DCs was detected by transmission electron microscopy. Western blotting was used to detect the protein levels of LC3, Beclin-1, P62, p-mTOR and p-Akt in DCs. TNF-α, IL-6 and IL-1β expression were investigated by ELISA. MiR-155 mimics were transfected to DCs to evaluate its effects on autophagy and cytokine production. RNA interference was used to downregulate the expression of TAB2.Results: The formation of autophagosomes was found in DCs of active BD patients. The expressions of LC3-Ⅱ, Beclin-1, P62, IL-6, IL-1β and TNF-α were significantly increased in DCs of active BD patients compared to that of healthy controls. The autophagy promoter (3-MA) and inhibitor (rapamycin) significantly decreased or increased the expression of TNF-α, IL-6 and IL-1β by DCs. The expression of LC3-Ⅱand Beclin-1 were significantly increased, but the expression of P62 proteins was decreased in DCs transfected with miR-155 mimics or after TAB2 was downregulated. The expression of TNF-α, IL-6 and IL-1β were decreased in DCs after miR-155 was upregulated or TAB2 was downregulated. The ratios of p-Akt/Akt and p-mTOR/mTOR were decreased in DCs after miR-155 was upregulated.Conclusions: These results suggest that miR-155 affects the production of TNF-α, IL-6 and IL-1β by DCs through activation of the Akt/mTOR signaling pathway and by affecting the process of autophagy.

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“…In this study, we have shown that paeonol, the main active compound of the traditionally used Chinese herb from Paeonia Suffruticosa Andrews, has VECs protective activities. A model of ox-LDL-impaired VECs has been applied to mimic the oxidative endothelial injury that occurs during atherogenesis ( Wu et al, 2016 ). Paeonol has protective effect on VECs exposed to ox-LDL by increasing VECs growth.…”

Section: Discussionmentioning

confidence: 99%

Paeonol Inhibits Oxidized Low-Density Lipoprotein-Induced Vascular Endothelial Cells Autophagy by Upregulating the Expression of miRNA-30a

Yang

et al. 2018

Front. Pharmacol.

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Paeonol from Cortex Moutan root is a potential therapeutic agent for atherosclerosis (AS). However, its mechanisms of action are still not fully understood. Vascular endothelial cells (VECs) autophagy plays a vital role in the initiation and progression of AS. In this study, we aim to investigate whether the protective effect of paeonol on ox-LDL-induced VECs injury by regulating autophagy. To address this question, we used ox-LDL-induced rat VECs as a model system to elucidate the protective effect of paeonol on VECs injury. This study displayed that ox-LDL (100 mg/L) treatment inhibited VEC growth in dose- and time-dependent manners, paeonol (60 μM) shown potential in inhibiting ox-LDL-induced death. Furthermore, paeonol significantly reduced ox-LDL-induced the formation of autophagy vacuoles and the expression of LC3II in VECs. Further double-luciferase reporter assay shown that miR-30a specifically binds to the 3′-UTR of Beclin-1 mRNA in VECs. Moreover, we found that ox-LDL decreased miR-30a and increased Beclin-1 expression, pretreatment with paeonol could reverse the process of regulation in dose-dependent manners. In ox-LDL treated VECs, transfection with a miR-30a mimic significantly increased miR-30a expression and inhibited Beclin-1 and LC3II expression, thus enhanced the protective effects of paeonol. Whereas transfection with a miR-30a inhibitor significantly decreased miR-30a expression and increased Beclin-1 and LC3II expression, thus attenuated the protective effects of paeonol. In conclusion, this study has, for the ?rst time, highlighted that miR-30a might be a critical target of paeonol against ox-LDL-induced VECs injury by inhibiting excessive autophagy. Paeonol may be one of promising candidate drug for treatment of AS.

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MicroRNA-155-enhanced autophagy in human gastric epithelial cell in response to Helicobacter pylori

Cited by 34 publications

References 19 publications

Expression and Function of miR-155 in Diseases of the Gastrointestinal Tract

Expression and Function of miR-155 in Diseases of the Gastrointestinal Tract

Decreased MicroRNA-155 in Behcet’s disease leads to defective control of autophagy thereby stimulating excessive proinflammatory cytokine production

Paeonol Inhibits Oxidized Low-Density Lipoprotein-Induced Vascular Endothelial Cells Autophagy by Upregulating the Expression of miRNA-30a

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