scholarly journals Long noncoding RNAs: novel links to inflammatory bowel disease?

2016 ◽  
Vol 311 (3) ◽  
pp. G444-G445 ◽  
Author(s):  
Laura E. Edgington-Mitchell
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Inflammatory Bowel

scholarly journals Which long noncoding RNAs and circular RNAs contribute to inflammatory bowel disease?

2020 ◽  
Vol 11 (6) ◽  
Author(s):  
Lihui Lin ◽  
Gaoshi Zhou ◽  
Peng Chen ◽  
Ying Wang ◽  
Jing Han ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Circular Rnas ◽  
Inflammatory Bowel

scholarly journals The Emerging Role of Noncoding RNAs in Pediatric Inflammatory Bowel Disease

2020 ◽  
Vol 26 (7) ◽  
pp. 985-993 ◽  
Author(s):  
Petr Jabandziev ◽  
Julia Bohosova ◽  
Tereza Pinkasova ◽  
Lumir Kunovsky ◽  
Ondrej Slaby ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Expression Profiles ◽  
Significant Proportion ◽  
Noncoding Rnas ◽  
Inflammatory Disorder ◽  
Altered Expression ◽  
Clinical Biomarkers ◽  
Inflammatory Bowel ◽  
Pediatric Ibd

Abstract Prevalence of inflammatory bowel disease (IBD), a chronic inflammatory disorder of the gut, has been on the rise in recent years—not only in the adult population but also especially in pediatric patients. Despite the absence of curative treatments, current therapeutic options are able to achieve long-term remission in a significant proportion of cases. To this end, however, there is a need for biomarkers enabling accurate diagnosis, prognosis, and prediction of response to therapies to facilitate a more individualized approach to pediatric IBD patients. In recent years, evidence has continued to evolve concerning noncoding RNAs (ncRNAs) and their roles as integral factors in key immune-related cellular pathways. Specific deregulation patterns of ncRNAs have been linked to pathogenesis of various diseases, including pediatric IBD. In this article, we provide an overview of current knowledge on ncRNAs, their altered expression profiles in pediatric IBD patients, and how these are emerging as potentially valuable clinical biomarkers as we enter an era of personalized medicine.

scholarly journals Epigenetic Regulation of Glycosylation in Cancer and Other Diseases

2021 ◽  
Vol 22 (6) ◽  
pp. 2980
Author(s):  
Rossella Indellicato ◽  
Marco Trinchera
Keyword(s):  
Dna Methylation ◽  
Inflammatory Bowel Disease ◽  
Transcription Factors ◽  
Epigenetic Regulation ◽  
Bowel Disease ◽  
Noncoding Rnas ◽  
Fine Tuning ◽  
Epigenetic Mechanisms ◽  
Complex Process ◽  
Inflammatory Bowel

In the last few decades, the newly emerging field of epigenetic regulation of glycosylation acquired more importance because it is unraveling physiological and pathological mechanisms related to glycan functions. Glycosylation is a complex process in which proteins and lipids are modified by the attachment of monosaccharides. The main actors in this kind of modification are the glycoenzymes, which are translated from glycosylation-related genes (or glycogenes). The expression of glycogenes is regulated by transcription factors and epigenetic mechanisms (mainly DNA methylation, histone acetylation and noncoding RNAs). This review focuses only on these last ones, in relation to cancer and other diseases, such as inflammatory bowel disease and IgA1 nephropathy. In fact, it is clear that a deeper knowledge in the fine-tuning of glycogenes is essential for acquiring new insights in the glycan field, especially if this could be useful for finding novel and personalized therapeutics.

scholarly journals Identification of novel mRNAs and lncRNAs associated with mouse experimental colitis and human inflammatory bowel disease

2018 ◽  
Vol 315 (5) ◽  
pp. G722-G733 ◽  
Author(s):  
Carl Robert Rankin ◽  
Evangelos Theodorou ◽  
Ivy Ka Man Law ◽  
Lorraine Rowe ◽  
Efi Kokkotou ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Models ◽  
High Throughput ◽  
Bowel Disease ◽  
Noncoding Rnas ◽  
Transcriptomic Analysis ◽  
Differentially Expressed ◽  
Clinical Samples ◽  
Rna Seq ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a complex disorder that is associated with significant morbidity. While many recent advances have been made with new diagnostic and therapeutic tools, a deeper understanding of its basic pathophysiology is needed to continue this trend toward improving treatments. By utilizing an unbiased, high-throughput transcriptomic analysis of two well-established mouse models of colitis, we set out to uncover novel coding and noncoding RNAs that are differentially expressed in the setting of colonic inflammation. RNA-seq analysis was performed using colonic tissue from two mouse models of colitis, a dextran sodium sulfate-induced model and a genetic-induced model in mice lacking IL-10. We identified 81 coding RNAs that were commonly altered in both experimental models. Of these coding RNAs, 12 of the human orthologs were differentially expressed in a transcriptomic analysis of IBD patients. Interestingly, 5 of the 12 of human differentially expressed genes have not been previously identified as IBD-associated genes, including ubiquitin D. Our analysis also identified 15 noncoding RNAs that were differentially expressed in either mouse model. Surprisingly, only three noncoding RNAs were commonly dysregulated in both of these models. The discovery of these new coding and noncoding RNAs expands our transcriptional knowledge of mouse models of IBD and offers additional targets to deepen our understanding of the pathophysiology of IBD. NEW & NOTEWORTHY Much of the genome is transcribed as non-protein-coding RNAs; however, their role in inflammatory bowel disease is largely unknown. This study represents the first of its kind to analyze the expression of long noncoding RNAs in two mouse models of inflammatory bowel disease and correlate them to human clinical samples. Using high-throughput RNA-seq analysis, we identified new coding and noncoding RNAs that were differentially expressed such as ubiquitin D and 5730437C11Rik.

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