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| 1 | miR-20b, miR-98, miR-125b-1*, and let-7e* as new potential diagnostic biomarkers in ulcerative colitis显示文摘AIM:To use microarray-based miRNA profiling of colonic mucosal biopsies from patients with ulcerative colitis (UC), Crohn's disease (CD), and controls in order to identify new potential miRNA biomarkers in inflammatory bowel disease. METHODS:Colonic mucosal pinch biopsies from the descending part were obtained endoscopically from patients with active UC or CD, quiescent UC or CD, as well as healthy controls. Total RNA was isolated and miRNA expression assessed using the miRNA microarray Geniom Biochip miRNA Homo sapiens (Febit GmbH, Heidelberg, Germany). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P+12 software package (Umetrics, Umea, Sweden). The microarray data were subsequently validated by quantitative real-time polymerase chain reaction (qPCR) performed on colonic tissue samples from active UC patients (n = 20), patients with quiescent UC (n = 19), and healthy controls (n = 20). The qPCR results were analyzed with Mann-WhitneyU test.In silico prediction analysis were performed to identify potential miRNA target genes and the predicted miRNA targets were then compared with all UC associated susceptibility genes reported in the literature. RESULTS:The colonic mucosal miRNA transcriptome differs significantly between UC and controls, UC and CD, as well as between UC patients with mucosal inflammation and those without. However, no clear differences in the transcriptome of patients with CD and controls were found. The miRNAs with the strongest differential power were identified (miR-20b, miR-99a, miR-203, miR-26b, and miR-98) and found to be upregulated more than a 10-fold in active UC as compared to quiescent UC, CD, and controls. Two miRNAs, miR-125b-1* and let-7e*, were up-regulated more than 5-fold in quiescent UC compared to active UC, CD, and controls. Four of the seven miRNAs (miR-20b, miR-98, miR-125b-1*, and let-7e*) were validated by qPCR and found to be specifically upregulated in patients with UC. Usingin silico analysis we found several predicted pro-inflammatory target genes involved in various pathways, such as mitogen-activated protein kinase and cytokine signaling, which are both key signaling pathways in UC.CONCLUSION:The present study provides the first evidence that miR-20b, miR-98, miR-125b-1*, and let7e* are deregulated in patients with UC. The level of these miRNAs may serve as new potential biomarkers for this chronic disease. | Mehmet Coskun Jacob Tveiten Bjerrum Jakob Benedict Seidelin Jesper Thorvald Troelsen JΦrgen Olsen Ole Haagen Nielsen | 2013 | World Journal of Gastroenterology2013，19，27： | 19 |
| 2 | MicroRNAs in inflammatory bowel disease-pathogenesis,diagnostics and therapeutics显示文摘The pathogenesis of inflammatory bowel disease (IBD) is complex and largely unknown. Until recently, research has focused on the study of protein regulators in inflammation to reveal the cellular and molecular networks in the pathogenesis of IBD. However, in the last few years, new and promising insights have been generated from studies describing an association between an altered expression of a specific class of non-coding RNAs, called microRNAs (miRs or miRNAs) and IBD. The short (approximately 22 nucleotides), endogenous, single-stranded RNAs are evolutionary conserved inanimals and plants, and regulate specific target mRNAs at the post-transcriptional level. MiRNAs are involved in several biological processes, including development, cell differentiation, proliferation and apoptosis. Furthermore, it is estimated that miRNAs may be responsible for regulating the expression of nearly one-third of the genes in the human genome. Thus, miRNA deregulation often results in an impaired cellular function, and a disturbance of downstream gene regulation and signaling cascades, suggesting their implication in disease etiology. Despite the identification of more than 1900 mature human miRNAs, very little is known about their biological functions and functional targets. Recent studies have identified dysregulated miRNAs in tissue samples of IBD patients and have demonstrated similar differences in circulating miRNAs in the serum of IBD patients. Thus, there is great promise that miRNAs will aid in the early diagnosis of IBD, and in the development of personalized therapies. Here, we provide a short review of the current state-of-the-art of miRNAs in IBD pathogenesis, diagnostics and therapeutics. | Mehmet Coskun Jacob Tveiten Bjerrum Jakob Benedict Seidelin Ole Haagen Nielsen | 2012 | World Journal of Gastroenterology2012，18，34： | 18 |
| 3 | Mucosal Healing in Ulcerative Colitis显示文摘 | Jakob Benedict Seidelin Mehmet Coskun Ole Haagen Nielsen | 2013 | Advances in Clinical Chemistry2013，，： | 2 |
| 4 | Mobilization within thirty minutes of elective diagnositic coronary angiography: a feasibility study using a hemostatic femor punction closure device显示文摘 | Seidelin PH Adelman AG | 1997 | Intervent Cardiol1997，10，： | 1 |
| 5 | IL-33 promotes GA- TA-3 polarization of gut-derived T cells in experimental and ulcerative colitis显示文摘 | Seidelin J B Coskun M Kvist P H | 2015 | J Gastroenterol2015，50，2： | 1 |
| 6 | Long-term endothelial dysfunction after coronary artery stenting显示文摘 | Caramori P Lima F Seidelin P | 1999 | J Am Coll Cardiol1999，34，： | 1 |
| 7 | Soluble L-selectin levels predict survival in sepsis显示文摘 | Seidelin JB Nielsen OH Strom J | 2002 | Intensive Care Med2002，28，11： | 1 |
| 8 | Creation of a Six-atom Schr dinger cat' State显示文摘 | LEIBFRIED D KNILL E SEIDELIN S | 2005 | Nature (London)2005，438，： | 1 |
| 9 | Insulin-like Growth Factor Binding Protein 3 in Inflammatory Bowel Disease显示文摘 | Irena Kirman Richard Larry Whelan Suvinit Jain Sara Els?e Nielsen Jakob Benedict Seidelin Ole Haagen Nielsen | 2005 | Digestive Diseases and Sciences2005，，4： | 1 |
| 10 | Biological treatment of Crohn's disease显示文摘 | Nielsen OH Bjerrum JT Seidelin JB | | 0，，03： | 1 |
| 11 | Tissue‐regenerating functions of coagulation factor XIII显示文摘 | C. Soendergaard P. H. Kvist J. B. Seidelin O. H. Nielsen | 2013 | J Thromb Haemost2013，，5： | 1 |
| 12 | Ventricular FibrillationPrecipitated by Intracoronary Adenosine During FractionalFlow Reserve Assessment-A Cautionary Tale 显示文摘 | Shah A Chan W Seidelin P H | 2015 | HeartLung & Circulation2015，24，： | 1 |
| 13 | Choice of stent and outcomes after treatment of drug‐eluting stent restenosis in highly complex lesions显示文摘 | Xavier Freixa Ali S. Almasood Sohail Q. Khan Karen Mackie Mark Osten Douglas Ing Christopher B. Overgaard Eric M. Horlick Peter H. Seidelin Vladimír D?avík | 2012 | Cathet Cardiovasc Intervent2012，，1： | 1 |
| 14 | Endocrine control of Na^+/ K^+-ATPase and chloride cell development in brown trout (Salmo trutta) :interaction of insulin-like growth factor-I with prolactin and growth hormone显示文摘 | Seidelin M Madsen S S | 1999 | Jour- nal of Endocrinology1999，162，1： | 1 |
| 15 | IL-33 is upregulated in colonoeytes of ulcerative colitis显示文摘 | Seidelin JB Bjermm JT Coskun M | 2010 | Immunol Lett2010，128，1： | 1 |
| 16 | Dynamics of Na^+, K^+, 2 Cl-cotransporter and Na^+, K^+-ATPasee expression in the branchial epithelium of brown trout(Salmo trotta) and Atlantic salmon (Salmo salar)显示文摘 | Tipsmark C K Madsem S S Seidelin M | 2002 | J Exp Zool2002，293，： | 1 |
| 17 | Inhibitors of apoptosis (IAPs) regulate intestinal immunity and inflammatory bowel disease (IBD) inflammation显示文摘 | Jannie Pedersen Eric C. LaCasse Jakob B. Seidelin Mehmet Coskun Ole H. Nielsen | 2014 | Trends in Molecular Medicine2014，，11： | 1 |
| 18 | IL-33 is upregnlated in colonocytes of ulcerative colitis显示文摘 | Seidelin JB Bjerrum JT Coskun M | 2010 | Immunol Lett2010，128，1： | 1 |
| 19 | Long-term outcomes after percutaneous cor- onary intervention of bifurcation nanowings 显示文摘 | Collins N Seidelin PH Daly P | 2008 | Am J Cardiol2008，102，4： | 1 |
| 20 | Safety of glycoprotein Ⅱ b/Ⅲ a inhibitors in urgent or emergency coronary artery bypass graft surgery显示文摘 | CHENG D K JACKEVICIUS C A SEIDELIN P | 2004 | Can J Cardiol2004，20，： | 1 |
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