Cadmium disorganises the scaffolding of gap and tight junction proteins in the hepatic cell line WIF B9

2013 ◽  
Vol 105 (12) ◽  
pp. 561-575 ◽  
Author(s):  
Sylviane Boucherie ◽  
Catherine Decaens ◽  
Jean-Marc Verbavatz ◽  
Brigitte Grosse ◽  
Marie Erard ◽  
...  
Keyword(s):  
Tight Junction ◽  
Cell Line ◽  
Hepatic Cell ◽  
Tight Junction Proteins ◽  
Hepatic Cell Line ◽  
Junction Proteins

scholarly journals Allyl Isothiocyanate Ameliorates Dextran Sodium Sulfate-Induced Colitis in Mouse by Enhancing Tight Junction and Mucin Expression

2018 ◽  
Vol 19 (7) ◽  
pp. 2025 ◽  
Author(s):  
Min Kim ◽  
Seungho Choi ◽  
Sun Kim ◽  
Yeo Yoon ◽  
Ju-Hee Kang ◽  
...  
Keyword(s):  
Tight Junction ◽  
Cell Line ◽  
Allyl Isothiocyanate ◽  
In Vivo Studies ◽  
Intestinal Barrier Function ◽  
Tight Junction Proteins ◽  
Mucin Expression ◽  
Junction Proteins

Inflammatory bowel disease (IBD) is characterized by chronic or recurrent inflammation of the gastrointestinal tract. Even though the current strategies to treat IBD include anti-inflammatory drugs and immune modulators, these treatments have side-effects. New strategies are, therefore, required to overcome the limitations of the therapies. In this study, we investigated the anti-colitic effects of allyl isothiocyanate (AITC), which is an active ingredient present in Wasabia japonica. The DSS-induced colitis model in the mouse was used to mimic human IBD and we observed that AITC treatment ameliorated the severity of colitis. We further studied the mechanism involved to ameliorate the colitis. To investigate the involvement of AITC on the intestinal barrier function, the effect on the intercellular tight junction was evaluated in the Caco-2 cell line while mucin expression was assessed in the LS174T cell line. AITC positively regulated tight junction proteins and mucin 2 (MUC2) against DSS-induced damage or depletion. Our data of in vivo studies were also consistent with the in vitro results. Furthermore, we observed that MUC2 increased by AITC is dependent on ERK signaling. In conclusion, we propose that AITC can be considered as a new strategy for treating IBD by modulating tight junction proteins and mucin.

Tight junction protein MAGI-1 is up-regulated by transfection with connexin 32 in an immortalized mouse hepatic cell line: cDNA microarray analysis

2004 ◽  
Vol 319 (2) ◽  
pp. 341-347 ◽  
Author(s):  
Masaki Murata ◽  
Takashi Kojima ◽  
Toshinobu Yamamoto ◽  
Mitsuru Go ◽  
Ken-ichi Takano ◽  
...  
Keyword(s):  
Tight Junction ◽  
Cell Line ◽  
Microarray Analysis ◽  
Cdna Microarray ◽  
Hepatic Cell ◽  
Tight Junction Protein ◽  
Connexin 32 ◽  
Cdna Microarray Analysis ◽  
Hepatic Cell Line ◽  
Junction Protein

Tight junction proteins in HCC and metastatic liver tumours

2005 ◽  
Vol 43 (05) ◽  
Author(s):  
Cs Páska ◽  
E Orbán ◽  
A Kiss ◽  
Zs Schaff ◽  
A Szijjártó ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Proteins ◽  
Liver Tumours ◽  
Metastatic Liver ◽  
Junction Proteins

Expression des Tight junction-Proteins Cingulin im humanen Gastrointestinaltrakt und korrespondierenden Karzinomen–Ein neuer Marker des epithelialen Differenzierungsgrades?

2005 ◽  
Vol 43 (05) ◽  
Author(s):  
UF Pape ◽  
I Eichhorn ◽  
L Langbein ◽  
I Hofmann ◽  
WW Franke ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Proteins ◽  
Junction Proteins

Evidence that gene expression of ovarian follicular tight junction proteins is regulated in vivo and in vitro in cattle

2017 ◽  
Vol 95 (3) ◽  
pp. 1313 ◽  
Author(s):  
L. Zhang ◽  
L. F. Schütz ◽  
C. L. Robinson ◽  
M. L. Totty ◽  
L. J. Spicer
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Tight Junction Proteins ◽  
Junction Proteins

Synthesis, Characterization and In vitro Evaluation of N-Substituted- Sulfomoyl-Phenyl-Amino Carboxylic Acid Derivatives as Squalene Synthase Inhibitors

2019 ◽  
Vol 15 (4) ◽  
pp. 415-426
Author(s):  
Avani B. Chokshi ◽  
Mahesh T. Chhabria ◽  
Pritesh R. Desai
Keyword(s):  
Carboxylic Acid ◽  
Cell Line ◽  
Hepatic Cell ◽  
Squalene Synthase ◽  
Lipid Lowering ◽  
Assay Method ◽  
Aromatic Substituent ◽  
Hepatic Cell Line ◽  
Amino Carboxylic Acid

Background:Squalene Synthase is one of the cholesterol biosynthetic pathway enzymes, inhibition of which produces potent lipid lowering action. A variety of chemical classes have been evaluated for its inhibition to provide alternate antihyperlipidemic agents to statins.Methods:A series of N-substituted-sulfomoyl-phenyl-amino carboxylic acid derivatives were designed through pharmacophore modelling as Squalene Synthase inhibitors. We report here the synthesis, characterization and in vitro pharmacological screening of the designed molecules as Squalene synthase inhibitors. The target molecules were synthesized by a simple procedure and each molecule was characterized by IR, Mass, 1HNMR and 13CNMR spectroscopic techniques. As a primary site of action for cholesterol biosynthesis is liver, each of the molecules were first screened for in vitro cytotoxicity over human hepatic cell line (HepG2) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay method. The enzyme inhibition assay was performed on cell lysates prepared from HepG2 cells by Human Squalene Synthase ELISA kit, where test compounds were added in the nontoxic concentrations only.Results:Compound 5f was found to be most potent with the IC50 value of 11.91 µM. The CTC50 value for 5f on human hepatic cell line was > 1000 µM so it was considered that the compound was relatively safe and might be free of hepatotoxicity.Conclusion:From the results of our studies, it was observed that compounds with poly nuclear aromatic or hetero aromatic substituent on a side chain were more potent enzyme inhibitors and a distance of 4-5 atoms is optimum between amide nitrogen and hydroxyl group of carboxylic acid.

New insights in gut-liver axis in wild-type murine imiquimod-induced lupus

Lupus ◽  
2021 ◽  
Vol 30 (6) ◽  
pp. 926-936
Author(s):  
Georges Maalouly ◽  
Joelle Hajal ◽  
Charbel Noujeim ◽  
Michel Choueiry ◽  
Hussein Nassereddine ◽  
...  
Keyword(s):  
Tight Junction ◽  
Fecal Calprotectin ◽  
Liver Inflammation ◽  
Tight Junction Proteins ◽  
Wild Type ◽  
Imiquimod Cream ◽  
E Coli ◽  
Intestinal Pathology ◽  
Nfκb Pathway ◽  
Junction Proteins

Background Intestinal and hepatic manifestations of lupus seem to be underestimated in comparison to other major organ lesions. Although recent data point to gut-liver axis involvement in lupus, gut permeability dysfunction and liver inflammation need to be more investigated. Objective This study aims to assess fecal calprotectin, intestinal tight junction proteins and liver inflammation pathway in wild-type murine imiquimod- induced lupus. Methods C57BL/6 mice were topically treated on their right ears with 1.25 mg of 5% imiquimod cream, three times per week for six weeks. Fecal calprotectin was collected at day 0, 22 and 45. Renal, liver and intestinal pathology, as well as inflammatory markers, intestinal tight junction proteins, and E. coli protein in liver were assessed at sacrifice. Results At six weeks, lupus nephritis was confirmed on histopathology and NGAL and KIM-1 expression. Calprotectin rise started at day 22 and persists at day 45. Protein expression of Claudine, ZO-1 and occludin was significantly decreased. E. coli protein was significantly increased in liver with necro-inflammation and increased TLR4, TLR7, and pNFκB/NFκB liver expression. Conclusion This study is the first to demonstrate early fecal calprotectin increase and liver activation of TLR4- NFκB pathway in wild-type murine imiquimod-induced lupus.

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