Novel specific microRNA biomarkers in idiopathic inflammatory bowel disease unrelated to disease activity

Ji, Lin; Welker, Noah C.; Zhao, Zijin; Li, Yong; Zhang, Jianjun; Reuss, Sarah; Zhang, Xinjun; Lee, Hwajeong; Liu, Yunlong; Bronner, Mary P.

doi:10.1038/modpathol.2013.152

Cited by 70 publications

(57 citation statements)

References 23 publications

(25 reference statements)

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“…Nguyen and colleagues [129] found that only miR7 was downregulated in eight active colonic CD patients compared to six healthy controls. In addition, miR206, miR424 [121] , miR106b [130] and miR196 [131] are also upregulated in active colonic CD. However, is there any tissuespecific miRNA expression profile in the gastrointestinal tract?…”

Section: Mirnas In CDmentioning

confidence: 97%

“…Furthermore, they found that miR192 participated in the regulation of chemokine production in colonic epithelial cells. Since 2008, some new research in active UC and healthy controls has confirmed the upregulation of miR-21 [25,118] , miR 29a [119] , and miR126 [120] , and identified additional upregulated miRNAs, including miR7, miR29b, miR126*, miR1273p, miR135b, miR223 and miR 3243p [119] , miR31 [119,121] , miR150 [26] , miR155 [118] , miR146a, miR206, and miR424 [121] , and miR 20b and miR125b1* [122] . In contrast, miR1885p, miR215, miR320a, miR346 [119] , and miR200b [123] were downregulated in colon tissues from active UC patients compared with healthy controls.…”

Section: Mirnas In Ucmentioning

confidence: 99%

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miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Zhang

2016

WJG

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Inflammatory bowel disease (IBD) is characterized by chronic relapsing inflammatory disorders of the gastrointestinal tract, and includes two major phenotypes: ulcerative colitis and Crohn's disease. The pathogenesis of IBD is not fully understood as of yet. It is believed that IBD results from complicated interactions between environmental factors, genetic predisposition, and immune disorders. miRNAs are a class of small non-coding RNAs that can regulate gene expression by targeting the 3′-untranslated region of specific mRNAs for degradation or translational inhibition. miRNAs are considered to play crucial regulatory roles in many biologic processes, such as immune cellular differentiation, proliferation, and apoptosis, and maintenance of immune homeostasis. Recently, aberrant expression of miRNAs was revealed to play an important role in autoimmune diseases, including IBD. In this review, we discuss the current understanding of how miRNAs regulate autoimmunity and inflammation by affecting the differentiation, maturation, and function of various immune cells. In particular, we focus on describing specific miRNA expression profiles in tissues and peripheral blood that may be associated with the pathogenesis of IBD. In addition, we summarize the opportunities for utilizing miRNAs as new biomarkers and as potential therapeutic targets in IBD.

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Section: Mirnas In CDmentioning

confidence: 97%

Section: Mirnas In Ucmentioning

confidence: 99%

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Zhang

2016

WJG

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“…106miRNAs are down regulated in UC, and 166 microRNAs are up regulated. Among the 106 down-regulated miRNAs, no miRNAs were consistently decreased more than 4 times (cut off>4).Among the 166 upregulated miRNAs, there is onlymiRNA-31 found increased in 5different studies (Olaru et al, 2011, Olaru et al, 2013, Coskun et al, 2013, Van der Goten et al, 2014, Lin et al, 2014, the total number of tissue samples were the addition of these five individual studies is 404, including 266 UC patients and 138 healthy volunteers. We also noticed that these selected miRNAs differentially expressed in a very inconsistent manner in these 10 profiling studies.…”

Section: Differentially Expressed Mirnasmentioning

confidence: 99%

“…Each of the published miRNA expression profiling studies comparing miRNA expression between inflamed and noninflamed control intestinal tissues provided a list of differentially expressed miRNAs (Wu et al, 2008, Fasseu et al, 2010, Takagi et al, 2010, Olaru et al, 2011, Olaru et al, 2013, Coskun et al, 2013, Van der Goten et al, 2014, Lin et al, 2014, Schaefer et al, 2015, Hubenthal et al, 2015. For example, Hubenthal et al (Hubenthal et al, 2015) carried out comprehensive analysis of UCrelated miRNAs based on a large number of miRNA profiling studies.…”

Section: Rankingmentioning

confidence: 99%

“…Beyond these, an important feature of miRNA is their remarkable stability, for example, they can be well preserved in tissue samples even after formalin-fixation and paraffin embedding for years, and can be efficiently extracted from such specimens and variety of cell lines (Finkel et al, 2007). Actually, several endeavors have been imposed to search for biomarkers or therapeutic agents by identifying the differentially expressed miRNAs between UC inflamed tissue and corresponding non-inflamed tissue (Wu et al, 2008, Fasseu et al, 2010, Takagi et al, 2010, Olaru et al, 2011, Olaru et al, 2013, Coskun et al, 2013, Van der Goten et al, 2014, Lin et al, 2014, Schaefer et al, 2015, Hubenthal et al, 2015. These studies generated hundreds of differentially expressed miRNAs, however, many of these are likely limited by different bias and finally only a small number of them may be of clinical significance and act as potential diagnostic agents.…”

Section: Introductionmentioning

confidence: 99%

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Over expressed miRNA-31 is the Most Consistent and Unique Micro RNA in Ulcerative Colitis

Cao¹,

Li²,

Li³

et al. 2016

Int.J.Curr.Res.Aca.Rev.

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A B S T R A C TRecently, several micro RNA (miRNA) profiling studies have been performed on ulcerative colitis (UC) tissues but with extremely inconsistency, their diagnostic or therapeutic value remains debate. Thus, this study aims to systematically evaluate the consistency of miRNAs from multiple independent studies. Eligible studies were collected from online programs, followed by a systematic analysis on miRNAs. Real time PCRs were employed to validate miRNA candidates. The target genes of high consistent miRNAs were collected with online programs. Enrichment analyses for gene ontology (GO) terms and Kyoto encyclopedia of genes and genomes (KEGG) pathways were carried out. A total of 272differentially expressed miRNAs were reported in 10 profiling studies, of which 166 were upregulated and 106 were down regulated. In the group of consistently up-regulated miRNAs (cutoff>4 times), miRNA-31 was the only miRNA found in 5 different studies. Among the 106 down-regulated miRNAs, none of them expressed consistently in more than 4 different studies. The increased miRNA-31 was confirmed by real-time PCR. Enrichment analyses demonstrated that the regulation of transcription and metabolic process play important roles during the interplay of miRNAs with UC. Conclusion: This systematic study demonstrates that pro-inflammatory miRNA-31 is the only consistently differently expressed miRNA.

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Retracted: Notoginsenoside R1 protects WI‐38 cells against lipopolysaccharide‐triggered injury via adjusting the miR‐181a/TLR4 axis

Qian

Shao

et al. 2019

J of Cellular Biochemistry

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Notoginsenoside R1 (NGR1) is a neoteric phytoestrogen extracted from Panax notoginseng, and possesses comprehensive pharmacological functions in multitudinous ailments. But, whether NGR1 is utilized in neonatal pneumonia is not clear. This research study aspired to disclose the protective activity of NGR1 in neonatal pneumonia. WI-38 cells were co-stimulated with NGR1 and lipopolysaccharide (LPS, 10 ng/mL), CCK-8 and flow cytometry assays were implemented for cell viability and apoptosis assessment. Real-time quantitative plymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and Western blot analysis were executed for inflammatory cytokine determination. MicroRNA-181a (miR-181a) expression was evaluated through RT-qPCR, simultaneously, the impact of miR-181a was estimated in NGR1 and LPS co-managed cells. Dual luciferase report assay was performed to disclose the relation between miR-181a and Toll-like receptor 4 (TLR4). The nuclear factor-κB (NF-κB) and TAK1/JNK pathways were ultimately appraised.We found that NGR1 decreased cell viability, evoked apoptosis and impeded interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) expression and secretions in LPS-managed WI-38 cells. MiR-181a expression was enhanced by NGR1, and miR-181a inhibition inverted the impacts of NGR1 in LPSmanaged WI-38 cells. Besides, TLR4 was predicted to be a firsthand direct target of miR-181a. Furthermore, NGR1 hindered NF-κB and TAK1/JNK pathways through modulating TLR4. These discoveries disclosed the fact that NGR1 protected WI-38 cells against LPS-triggered injury via adjusting the miR-181a/ TLR4 and NF-κB and TAK1/JNK pathways. K E Y W O R D SmicroRNA-181a, neonatal pneumonia, NF-κB, notoginsenoside R1, TAK1/JNK, toll-like receptor 4 | INTRODUCTIONNeonatal pneumonia is a universal ailment among newborns, and is also a major reason for neonatal death. 1 Statistical evidence displays that about 156 million new events of neonatal pneumonia take place around the world each year, and 95% of neonatal pneumonia episodes happen in the developing countries. 2 The clinical manifestations of neonatal pneumonia comprise fever, cough, dyspnea, heart failure, sepsis, and even death. 3,4 The causes of neonatal pneumonia are multitudinous and are linked to malnutrition, unsafe sanitation,

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Novel specific microRNA biomarkers in idiopathic inflammatory bowel disease unrelated to disease activity

Cited by 70 publications

References 23 publications

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Over expressed miRNA-31 is the Most Consistent and Unique Micro RNA in Ulcerative Colitis

Retracted: Notoginsenoside R1 protects WI‐38 cells against lipopolysaccharide‐triggered injury via adjusting the miR‐181a/TLR4 axis

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