scholarly journals Angiopoietin-2 silence alleviates lipopolysaccharide-induced inflammation, barrier dysfunction and endoplasmic reticulum stress of intestinal epithelial cells by blocking Notch signaling pathway

Bioengineered ◽  
2021 ◽  
Author(s):  
Liying Dai ◽  
Shuangshuang Jie ◽  
Shaohua Bi ◽  
Qing Qing ◽  
Jun Chen ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Intestinal Epithelial Cells ◽  
Notch Signaling Pathway ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Angiopoietin 2

scholarly journals Exosomes derived from Hp-positive gastritis patients inhibit MCP-1 and MIP-1α expression in intestinal epithelial cells and improve DSS-induced colitis in mice

2020 ◽  
Author(s):  
Yufan Chen ◽  
Jie-Bin Huang ◽  
Hao Li ◽  
Pu Li ◽  
Chun-Di Xu
Keyword(s):  
Epithelial Cells ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Chronic Gastritis ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Notch Signaling Pathway ◽  
Intestinal Epithelial ◽  
Protective Function ◽  
Serum Exosomes

Abstract Background: Previous studies have suggested that Helicobacter pylori (H. pylori, Hp) infection has a protective function in inflammatory bowel disease (IBD); Exosomes (Exo) are novel cell-cell communication mediators and their association with inflammatory immune responses has received great attention. however the mechanisms regarding the role of exosomes between Hp infection and IBD are limited.Methods: Human intestinal epithelial cells were treated with serum exosomes derived from Hp-positive chronic gastritis patients (Exo(Hp)), the expression of cytokines, inflammasome and signal pathway genes were detected by antibody microarray or PCR array. Furthermore, DSS-induced colitis mice were treated with exosomes by intraperitoneally injection to study the effect of Exo(Hp) in IBD.Results: Serum exosomes derived from Hp-positive chronic gastritis patients promoted NLRP12 expression in intestinal epithelial cells, and NLRP12 decreased chemokine MCP-1 and MIP-1α expression by inhibiting the Notch signaling pathway. In vivo, Exo(Hp) could attenuated inflammatory responses in DSS-induced colitis and improved colitis symptoms, which was associated with the increase in NLRP12 expression. Furthermore, the immunohistochemistry results showed that NLRP12 was negatively correlated with the disease activity of pediatric IBD patients. Conclusions: Exo(Hp) inhibited the Notch signaling pathway through the promotion of NLRP12 expression to further down-regulate MCP-1 and MIP-1α expression in intestinal epithelial cells and thereby attenuate DSS-induced colitis in mice. These results provide new theoretical bases for further elucidation of the intestinal protection mechanisms of Hp infection in IBD, and provide new targets for explorations of effective interventional strategies for IBD.

scholarly journals Effect of Berberine from Coptis chinensis on Apoptosis of Intestinal Epithelial Cells in a Mouse Model of Ulcerative Colitis: Role of Endoplasmic Reticulum Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Shen Yan ◽  
Liu Yingchao ◽  
Wang Zhangliu ◽  
Ruan Xianli ◽  
Li Si ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Caspase 3 ◽  
Intestinal Epithelial Cells ◽  
High Dose ◽  
Intestinal Epithelial ◽  
Model Group ◽  
Caspase 12

The purpose of this study was to verify the effect of berberine (BBR) on endoplasmic reticulum stress (ERS) and apoptosis of intestinal epithelial cells (IECs) in mice with ulcerative colitis (UC). BALB/c mice were randomly divided into five groups as follows: blank control, model, and low-, medium-, and high-dose BBR. A dextran sodium sulfate- (DSS-) induced model of UC was prepared, and the low-, medium-, and high-dose BBR groups were simultaneously gavaged with a BBR suspension for 7 d. Disease activity index (DAI) was assessed, and tissue damage index (TDI) was assessed from colon samples after the last administration. TUNEL assays were used to detect apoptosis of IECs. Immunohistochemistry and/or real-time PCR were applied to determine the expression of GRP78, caspase-12, and caspase-3. In all BBR treatment groups, clinical symptoms of colitis and histopathological damage were significantly reduced. The high-dose BBR group exhibited particularly pronounced decrease (p<0.01) in both DAI (0.48 ± 0.36) and TDI (1.62 ± 0.64) relative to the model group (1.50 ± 0.65 and 3.88 ± 0.04, respectively). In colon tissues of the model group, the number of apoptotic IECs was significantly increased; the expression of GRP78, caspase-12, and caspase-3 proteins was significantly increased; and the expression of the GRP78 mRNA was upregulated. In low-, medium-, and high-dose BBR groups, the number of apoptotic IECs was significantly reduced. Moreover, GRP78 and caspase-3 expression levels were significantly decreased in the medium- and high-dose BBR groups, caspase-12 expression was significantly decreased in the high-dose BBR group, and the GRP78 mRNA expression level was significantly decreased in the high-dose BBR group. BBR can effectively reduce the rate of IEC apoptosis in UC mice and alleviate the inflammatory response in the colon. The underlying mechanism seems to involve ERS modulation and inhibition of ERS-mediated activation of the caspase-12/caspase-3 apoptosis signaling pathway.

scholarly journals Crosstalk Between Nuclear Glucose-Regulated Protein 78 and Tumor Protein 53 Contributes to the Lipopolysaccharide Aggravated Apoptosis of Endoplasmic Reticulum Stress-Responsive Porcine Intestinal Epithelial Cells

2018 ◽  
Vol 48 (6) ◽  
pp. 2441-2455 ◽  
Author(s):  
Qian Jiang ◽  
Gang Liu ◽  
Jiashun Chen ◽  
Kang Yao ◽  
Yulong Yin
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cells ◽  
Intestinal Epithelial ◽  
Gram Negative ◽  
Rna Transfection ◽  
Glucose Regulated Protein

Background/Aims: Lipopolysaccharides (LPSs) act as virulence factors that trigger intestinal inflammation and thereby compromise the production of pigs worldwide. Intestinal diseases and dysfunction have been attributed to endoplasmic reticulum stress (ERS) and the subsequent apoptosis of intestinal epithelial cells. Therefore It is important to explore whether LPSs aggravate ERS-mediated apoptosis of intestinal epithelial cells. Methods: ERS and inflammation models were established in porcine cell line J2 (IPEC-J2) and the cells were treated with tunicamycin or LPS at specific times. The expression of marker proteins was determined by western blot and immunofluorescence. Possible crosstalk between proteins was analyzed by co-immunoprecipitation. Small interfering RNA transfection was employed to verify the mechanisms. Results: We found that Escherichia coli-derived LPS aggravated ERS and ERS-mediated apoptosis in ERS-responsive IPEC-J2 cells. The crosstalk between nuclear glucose-regulated protein 78 (GRP78) and tumor protein 53 (p53) was verified to trigger this LPS-aggravated apoptosis of ERS-responsive intestinal cells. Conclusion: This novel finding implies that intestinal malfunctions might solely originate from the effects of Gram-negative bacteria on ERS-responsive intestinal cells. The regulation of ERS signaling (especially the crosstalk between nuclear GRP78 and p53) in ERS-responsive/rapidly growing intestines may help intestinal cells survive from Gram-negative bacterial infections.

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