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Condition: Inflammatory Bowel Disease

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Total 147 results found since Jan 2013.

CDX2 upregulates SLC26A3 gene expression in intestinal epithelial cells
SLC26A3 [downregulated in adenoma (DRA)] plays a key role in mammalian intestinal NaCl absorption, in that it mediates apical membrane Cl–/HCO3– exchange. DRA function and expression are significantly decreased in diarrhea associated with inflammatory bowel disease. DRA is also considered to be a marker of cellular differentiation and is predominantly expressed in differentiated epithelial cells. Caudal-type homeobox protein-2 (CDX2) is known to regulate genes involved in intestinal epithelial differentiation and proliferation. Reduced expression of both DRA and CDX2 in intestinal inflammation prompted us to st...
Source: AJP: Gastrointestinal and Liver Physiology - September 1, 2017 Category: Gastroenterology Authors: Chatterjee, I., Kumar, A., Castilla-Madrigal, R. M., Pellon-Cardenas, O., Gill, R. K., Alrefai, W. A., Borthakur, A., Verzi, M., Dudeja, P. K. Tags: RESEARCH ARTICLE Source Type: research

Expression of Human Cathelicidin Peptide LL ‐37 in Inflammatory Bowel Disease
This article is protected by copyright. All rights reserved.
Source: Clinical and Experimental Immunology - September 1, 2017 Category: Allergy & Immunology Authors: Shoko Kusaka, Atsushi Nishida, Kenichiro Takahashi, Shigeki Bamba, Hiroyuki Yasui, Masahiro Kawahara, Osamu Inatomi, Mitsushige Sugimoto, Akira Andoh Tags: Original Article Source Type: research

Trimethylamine N-oxide prime NLRP3 inflammasome via inhibiting ATG16L1-induced autophagy in colonic epithelial cells.
This study observed the expression of ATG16L1, LC3-II and p62 and activation of NLRP3 inflammasome stimulated by TMAO in fetal human colon cells (FHCs), aiming to elucidate the mechanism by which the TMAO may contribute to colonic epithelial inflammation. Our results demonstrated that TMAO significantly inhibited ATG16L1, LC3-II and p62 expression, and triggered the activated NLRP3 inflammasome and production of ROS in a dose- and time-dependent manner. Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TM...
Source: Biochemical and Biophysical Research communications - August 2, 2017 Category: Biochemistry Authors: Yue C, Yang X, Li J, Chen X, Zhao X, Chen Y, Wen Y Tags: Biochem Biophys Res Commun Source Type: research

Oral administration of ginger-derived nanolipids loaded with siRNA as a novel approach for efficient siRNA drug delivery to treat ulcerative colitis
Nanomedicine Ahead of Print.
Source: Future Medicine: Nanomedicine - June 30, 2017 Category: Nanotechnology Source Type: research

CDX2 upregulates SLC26A3 gene expression in intestinal epithelial cells.
Abstract SLC26A3 (Down Regulated in Adenoma, DRA) plays a key role in mammalian intestinal NaCl absorption via mediating apical membrane Cl(-)/HCO3(-) exchange. DRA function and expression are significantly decreased in diarrhea associated with inflammatory bowel diseases (IBD). DRA is also considered to be a marker of cellular differentiation, and is predominantly expressed in differentiated epithelial cells. Caudal type homeobox protein-2 (CDX2) is known to regulate genes involved in intestinal epithelial differentiation and proliferation. Reduced expression of both DRA and CDX2 in intestinal inflammation prompt...
Source: American Journal of Physiology. Gastrointestinal and Liver Physiology - June 1, 2017 Category: Physiology Authors: Chatterjee I, Kumar A, Castilla Madrigal RM, Pellon-Cardenas O, Gill RK, Alrefai WA, Borthakur A, Verzi M, Dudeja PK Tags: Am J Physiol Gastrointest Liver Physiol Source Type: research

Orphan nuclear receptor Nur77 inhibits Poly (I:C)-triggered acute liver inflammation by inducing the ubiquitin-editing enzyme A20.
Authors: Li XM, Yang TY, He XS, Wang JR, Gan WJ, Zhang S, Li JM, Wu H Abstract Inflammation is a key contributor to various types of acute and chronic liver disease. We recently reported that lack of Nur77, an orphan nuclear receptor, contributes to the pathogenesis of inflammatory diseases including inflammatory bowel disease and sepsis. However, whether Nur77 plays a critical role in liver inflammation remains to be fully understood. Employing in vivo acute liver inflammation model in wild-type (Nur77+/+) and Nur77-/- mice, we here found that Nur77 deficiency dramatically increased the production of pro-inflammat...
Source: Oncotarget - May 26, 2017 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

P.05.4: Cancer Progression Control in Inflammatory Bowel Disease: Cyclin D1 and E2F1 Sirna Delivery by New Vectors
Source: Digestive and Liver Disease - March 15, 2017 Category: Gastroenterology Authors: I. Russo, S. Bochicchio, O. Piazza, A.A. Barba, G. Lamberti, A. Carrizzo, P. Zeppa, C. Vecchione, P. Iovino, C. Ciacci Tags: Posters Source Type: research

Chromosome region maintenance-1 (CRM1) regulates apoptosis of intestinal epithelial cells via p27kip1 in Crohn's disease
Conclusions Up-regulated CRM1 may facilitate IEC apoptosis possibly through p27kip1 in CD, indicating an important role of CRM1 in the pathophysiology of CD.
Source: Clinics and Research in Hepatology and Gastroenterology - March 9, 2017 Category: Gastroenterology Source Type: research

GWAS for serum galactose-deficient IgA1 implicates critical genes of the < i > O < /i > -glycosylation pathway
by Krzysztof Kiryluk, Yifu Li, Zina Moldoveanu, Hitoshi Suzuki, Colin Reily, Ping Hou, Jingyuan Xie, Nikol Mladkova, Sindhuri Prakash, Clara Fischman, Samantha Shapiro, Robert A. LeDesma, Drew Bradbury, Iuliana Ionita-Laza, Frank Eitner, Thomas Rauen, Nicolas Maillard, Francois Berthoux, J ürgen Floege, Nan Chen, Hong Zhang, Francesco Scolari, Robert J. Wyatt, Bruce A. Julian, Ali G. Gharavi, Jan Novak AberrantO-glycosylation of serum immunoglobulin A1 (IgA1) represents a heritable pathogenic defect in IgA nephropathy, the most common form of glomerulonephritis worldwide, but specific genetic factors involved in its dete...
Source: PLoS Genetics - February 9, 2017 Category: Genetics & Stem Cells Authors: Krzysztof Kiryluk Source Type: research

Microtubule-associated protein 1S-related autophagy inhibits apoptosis of intestinal epithelial cells via Wnt/ β-catenin signaling in Crohn's disease.
Microtubule-associated protein 1S-related autophagy inhibits apoptosis of intestinal epithelial cells via Wnt/β-catenin signaling in Crohn's disease. Biochem Biophys Res Commun. 2017 Feb 07;: Authors: Bai W, Bai J, Li Y, Tian D, Shi R Abstract Many autophagy-related genes, to our knowledge, have been identified as Crohn's disease (CD) polymorphic sites by genomic wide studies. As a novel member of the microtubule-associated protein 1 (MAP1) family, MAP1S is a microtubule-binding proteins involved in autophagy. However, its expression and potential functions in CD have not been understood. For the fir...
Source: Biochemical and Biophysical Research communications - February 6, 2017 Category: Biochemistry Authors: Bai W, Bai J, Li Y, Tian D, Shi R Tags: Biochem Biophys Res Commun Source Type: research

miRNA-133a-UCP2 pathway regulates inflammatory bowel disease progress by influencing inflammation, oxidative stress and energy metabolism.
CONCLUSION: The miR-133a-UCP2 pathway participates in IBD by altering downstream inflammation, oxidative stress and markers of energy metabolism, which provides novel clues and potential therapeutic targets for IBD. PMID: 28104982 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - January 6, 2017 Category: Gastroenterology Authors: Jin X, Chen D, Zheng RH, Zhang H, Chen YP, Xiang Z Tags: World J Gastroenterol Source Type: research

GPR4 deficiency alleviates intestinal inflammation in a mouse model of acute experimental colitis
Publication date: February 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1863, Issue 2 Author(s): Edward J. Sanderlin, Nancy R. Leffler, Kvin Lertpiriyapong, Qi Cai, Heng Hong, Vasudevan Bakthavatchalu, James G. Fox, Joani Zary Oswald, Calvin R. Justus, Elizabeth A. Krewson, Dorcas O’Rourke, Li V. Yang GPR4 is a proton-sensing G protein-coupled receptor that can be activated by extracellular acidosis. It has recently been demonstrated that activation of GPR4 by acidosis increases the expression of numerous inflammatory and stress response genes in vascular endothelial cells (ECs) a...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - December 11, 2016 Category: Molecular Biology Source Type: research

MicroRNA-206 is involved in the pathogenesis of ulcerative colitis via regulation of adenosine A3 receptor.
Authors: Wu W, He Y, Feng X, Ye S, Wang H, Tan W, Yu C, Hu J, Zheng R, Zhou Y Abstract Increasing evidence suggests that miRNAs are widely dysregulated in ulcerative colitis (UC), potentially affecting UC pathogenesis, diagnosis, and therapy. microRNA (miR) -206 has been reported to be upregulated in UC; however, its function and role in UC remain unknown. Here, we elucidate the function of miR-206 in the pathogenesis of UC. In patients with active-UC, miR-206 and adenosine A3 receptor (A3AR) levels were significantly upregulated and downregulated, respectively, and were inversely correlated. A3AR was expressed in ...
Source: Oncotarget - November 29, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Differential effects of {alpha}4{beta}7 and GPR15 on homing of effector and regulatory T cells from patients with UC to the inflamed gut in vivo
Conclusions α4β7 rather than GPR15 is crucial for increased colonic homing of UC Treg cells in vivo, while both receptors control UC Teff cell homing. Vedolizumab treatment impairs homing of UC Treg cells leading to their accumulation in peripheral blood with subsequent suppression of systemic Teff cell expansion.
Source: Gut - September 7, 2016 Category: Gastroenterology Authors: Fischer, A., Zundler, S., Atreya, R., Rath, T., Voskens, C., Hirschmann, S., Lopez-Posadas, R., Watson, A., Becker, C., Schuler, G., Neufert, C., Atreya, I., Neurath, M. F. Tags: Open access Inflammatory bowel disease Source Type: research