• Biomedical Science Letters
• /
• v.27 no.2
• /
• pp.77-87
• /
• 2021

Reflux esophagitis (RE) is a disease that stomach contents, stomach acid, and pepsin continually refluxing and is curently increasing worldwide. This study was conducted to find natural materials that can reduce side effects and effectively treat RE. Animal experiments were conducted with a 1:1 (EA1), 1:5 (EA5) ratio of Evodiae Fructus and Arecae Semen known to be effective against reflux esophagitis. As a result of confirming the total lesion of the esophageal mucosa after EA1 or EA5 treatment in reflux esophagitis animals, it showed superior improvement compared to the RE-control rats. In addition, by regulating the expression of MPO and NADPH oxidase, the activation of NF-κB was inhibited, and the expression of COX-1 and COX-2 was regulated. Moreover, its improved esophageal barrier function through regulating protein expressions of tight junction protein and MMPs/TIMPs. Taken together, a mixture of Evodiae Fructus and Arecae Semen can attenuate the damage to the esophageal mucosa that not only inactivationed the NF-κB through oxidative stress control, but also by regulating tight junctions and MMPs/TIMPs. This effect was more excellent in the 1:1 mixture (EA1) than in the Evodiae Fructus and Arecae Semen 1:5 mixture (EA5).

• Journal of Animal Reproduction and Biotechnology
• /
• v.36 no.4
• /
• pp.307-313
• /
• 2021

Traf4 (Tumor necrosis factor Receptor Associated Factor 4) is a member of the tumor necrosis factor receptor (TNFR) - associated factors (TRAFs) family. TRAF4 is overexpressed in tumor cells such as breast cancer and associated with cytoskeleton and membrane fraction. Interestingly, TRAF4 was localized with tight junctions (TJs) proteins including OCLN and TJP1 in mammary epithelial cells. However, the expression patterns and biological function of Traf4 were not examined in preimplantation mouse embryos although Traf4-deficient mouse showed embryonic lethality or various dramatic malformation. In this study, we examined the temporal and spatial expression patterns of mouse Traf4 during preimplantation development by qRT-PCR and immunostaining, and its biological function by using siRNA injection. We found upregulation of Traf4 from the 8-cell stage onwards and apical region of cell - cell contact sites at morula and blastocyst embryos. Moreover, Traf4 knockdown led to defective TJs without alteration of genes associated with TJ assembly but elevated p21 expression at the KD morula. Taken together, Traf4 is required for TJs assembly and cell proliferation during morula to blastocyst transition.

• Journal of Animal Science and Technology
• /
• v.64 no.5
• /
• pp.842-853
• /
• 2022

Ochratoxin A (OTA) is a well-known mycotoxin that causes disease through the ingestion of contaminated food or feed, for example, in the porcine industry. The intestinal epithelium acts as the first barrier against food contamination. We conducted a study on the exposure of the porcine intestinal epithelium to OTA. We used the intestinal porcine epithelial cell line IPEC-J2 as an in vitro model to evaluate the altered molecular mechanisms following OTA exposure. Gene expression profiling revealed that OTA upregulated 782 genes and downregulated 896, totalling 1678 differentially expressed genes. Furthermore, immunofluorescence, quantitative real-time polymerase chain reaction, and western blotting confirmed that OTA damages the tight junction protein ZO-1. Moreover, OTA activated the expression of inflammatory genes (IL-6, IL-8, IL-10, NF-kB, TLR4, and TNF-α). In summary, this study confirmed that OTA alters various molecular mechanisms and has several adverse effects on IPEC-J2 cells.

• Gut and Liver
• /
• v.12 no.6
• /
• pp.682-693
• /
• 2018

Background/Aims: Intestinal barrier dysfunction is a hallmark of inflammatory bowel diseases (IBDs) such as ulcerative colitis. This dysfunction is caused by increased permeability and the loss of tight junctions in intestinal epithelial cells. The aim of this study was to investigate whether estradiol treatment reduces colonic permeability, tight junction disruption, and inflammation in an azoxymethane (AOM)/dextran sodium sulfate (DSS) colon cancer mouse model. Methods: The effects of $17{\beta}$-estradiol (E2) were evaluated in ICR male mice 4 weeks after AOM/DSS treatment. Histological damage was scored by hematoxylin and eosin staining and the levels of the colonic mucosal cytokine myeloperoxidase (MPO) were assessed by enzyme-linked immunosorbent assay (ELISA). To evaluate the effects of E2 on intestinal permeability, tight junctions, and inflammation, we performed quantitative real-time polymerase chain reaction and Western blot analysis. Furthermore, the expression levels of mucin 2 (MUC2) and mucin 4 (MUC4) were measured as target genes for intestinal permeability, whereas zonula occludens 1 (ZO-1), occludin (OCLN), and claudin 4 (CLDN4) served as target genes for the tight junctions. Results: The colitis-mediated induced damage score and MPO activity were reduced by E2 treatment (p<0.05). In addition, the mRNA expression levels of intestinal barrier-related molecules (i.e., MUC2, ZO-1, OCLN, and CLDN4) were decreased by AOM/DSS-treatment; furthermore, this inhibition was rescued by E2 supplementation. The mRNA and protein expression of inflammation-related genes (i.e., KLF4, NF-${\kappa}B$, iNOS, and COX-2) was increased by AOM/DSS-treatment and ameliorated by E2. Conclusions: E2 acts through the estrogen receptor ${\beta}$ signaling pathway to elicit anti-inflammatory effects on intestinal barrier by inducing the expression of MUC2 and tight junction molecules and inhibiting pro-inflammatory cytokines.

• Proceedings of the PSK Conference
• /
• 2002.04a
• /
• pp.178.2-179
• /
• 2002

• Journal of the Society of Cosmetic Scientists of Korea
• /
• v.48 no.2
• /
• pp.181-188
• /
• 2022

The skin protects the body from excessive water loss and the invasion of harmful substances, such as chemicals and microbes. The stratum corneum, is recognized as a very important physical barrier. However, in recent years evidence emerged that tight junctions (TJ) might also play a crucial role in barrier function of the skin. In the present study, TJ proteins including transmembrane proteins and plaque proteins, skin permeability barrier function and skin diseases of TJ were reviewed.

• Proceedings of the PSK Conference
• /
• 2003.04a
• /
• pp.291.2-292
• /
• 2003

The purpose of this study was to investigate the transport characteristics of passage cultured l1uman nasal epithelial cell monolayers grown on Transwell@ inserts using liquid-covered culture (LCC) method. The monolayer of passage 2 and 3 exhibited tight barrier (TEER>1,000 ohmxcm$^2$) in 2-3 days after seeding. In the morphological studies by actin staining and SEM/TEM, the existence of tight junction was clearly observed. (omitted)

• Asian-Australasian Journal of Animal Sciences
• /
• v.29 no.5
• /
• pp.731-738
• /
• 2016

Glucagon-like peptide-2 (GLP-2) is important for intestinal barrier function and regulation of tight junction (TJ) proteins, but the intracellular mechanisms of action remain undefined. The purpose of this research was to determine the protective effect of GLP-2 mediated TJ and transepithelial electrical resistance (TER) in lipopolysaccharide (LPS) stressed IPEC-J2 cells and to test the hypothesis that GLP-2 regulate TJ and TER through the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway in IPEC-J2 cells. Wortmannin and LY294002 are specific inhibitors of PI3K. The results showed that $100{\mu}g/mL$ LPS stress decreased TER and TJ proteins occludin, claudin-1 and zonula occludens protein 1 (ZO-1) mRNA, proteins expressions (p<0.01) respectively. GLP-2 (100 nmol/L) promote TER and TJ proteins occludin, claudin-1, and zo-1 mRNA, proteins expressions in LPS stressed and normal IPEC-J2 cells (p<0.01) respectively. In normal cells, both wortmannin and LY294002, PI3K inhibitors, prevented the mRNA and protein expressions of Akt and mTOR increase induced by GLP-2 (p<0.01) following with the significant decreasing of occludin, claudin-1, ZO-1 mRNA and proteins expressions and TER (p<0.01). In conclusion, these results indicated that GLP-2 can promote TJ's expression and TER in LPS stressed and normal IPEC-J2 cells and GLP-2 could regulate TJ and TER through the PI3K/Akt/mTOR pathway.

• Asian-Australasian Journal of Animal Sciences
• /
• v.27 no.5
• /
• pp.733-742
• /
• 2014

The glucagon-like peptide 2 (GLP-2) that is expressed in intestine epithelial cells of mammals, is important for intestinal barrier function and regulation of tight junction (TJ) proteins. However, there is little known about the intracellular mechanisms of GLP-2 in the regulation of TJ proteins in piglets' intestinal epithelial cells. The purpose of this study is to test the hypothesis that GLP-2 regulates the expressions of TJ proteins in the mitogen-activated protein kinase (MAPK) signaling pathway in piglets' intestinal epithelial cells. The jejunal tissues were cultured in a Dulbecco's modified Eagle's medium/high glucose medium containing supplemental 0 to 100 nmol/L GLP-2. At 72 h after the treatment with the appropriate concentrations of GLP-2, the mRNA and protein expressions of zonula occludens-1 (ZO-1), occludin and claudin-1 were increased (p<0.05). U0126, an MAPK kinase inhibitor, prevented the mRNA and protein expressions of ZO-1, occludin, claudin-1 increase induced by GLP-2 (p<0.05). In conclusion, these results indicated that GLP-2 could improve the expression of TJ proteins in weaned pigs' jejunal epithelium, and the underlying mechanism may due to the MAPK signaling pathway.

• BMB Reports
• /
• v.42 no.10
• /
• pp.655-660
• /
• 2009

The potential anti-metastasis and anti-invasion activities of early growth response gene-1 (Egr-1) and claudin-3, a tight junction (TJ)-related protein, were evaluated using histone deacetylase (HDAC) inhibitors in human hepatocarcinoma cells. The results of wound healing and Transwell assays showed that HDAC inhibitors such as trichostatin A and sodium butyrate inhibited cell migration and invasion. HDAC inhibitors markedly induced Egr-1 expression during the early period, after which expression levels decreased. In addition, the down-regulation of snail and type 1 insulin-like growth factor receptor (IGF-1R) in HDAC inhibitor- treated cells induced the upregulation of thrombospondin-1 (TSP-1), E-cadherin and claudin-3. Cells transfected with Egr-1 and claudin-3 siRNA displayed significant blockage of HDAC inhibitor-induced anti-invasive activity. Collectively, these findings indicate that the up-regulation of Egr-1 and claudin-3 are crucial steps in HDAC inhibitor-induced anti-metastasis and anti-invasion.