miR-122 targets NOD2 to decrease intestinal epithelial cell injury in Crohn’s disease

Chen, Yu; Wang, Chengxiao; Liu, Ying; Tang, Liwei; Zheng, Maojun; Che, Xu; Song, Jinsup; Meng, Xiaochun

doi:10.1016/j.bbrc.2013.07.040

Cited by 85 publications

(50 citation statements)

References 29 publications

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“…A miRs NOD interaction has been implicated in IBD. These miRNAs include miR29 [65] , miR122 [66] , miR146a [67] , and miR192 [68] . For example, polymorphisms in NOD2 impair miR29 expression in DCs, and this results in exaggerated IL-23-induced inflammation [65] .…”

Section: Nod-like Receptorsmentioning

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: Nod-like Receptorsmentioning

confidence: 99%

“…For example, polymorphisms in NOD2 impair miR29 expression in DCs, and this results in exaggerated IL-23-induced inflammation [65] . miR122 targeting of NOD2 has a crucial role in the damage of intestinal epithelial cells induced by lipopoly saccharide [66] .…”

Section: Nod-like Receptorsmentioning

confidence: 99%

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

Zhang

2016

WJG

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“…Using a HT-29 ex vivo colon epithelial cell culture system, Chen and colleagues identified miR-122 targeting of NOD2, inhibiting innate immune system activation via the NF-κB pathway [Chen et al 2013a [Sandborn et al 2012], one may be able extrapolate the efficacy of miR-29 mimicry as another mechanism to reduce IL-23 production. With regard to potential off-target effects, miR-29a and -29c have been reported to be tumor suppressors across multiple malignancies [Bae et al 2014].…”

Section: Nod2mentioning

confidence: 99%

The emerging role of miRNAs in inflammatory bowel disease: a review

Chapman

Pekow

2014

Therap Adv Gastroenterol

132

106

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Inflammatory bowel disease (IBD), comprised of ulcerative colitis and Crohn's disease, is believed to develop as a result of a deregulated inflammatory response to environmental factors in genetically susceptible individuals. Despite advances in understanding the genetic risks of IBD, associated single nucleotide polymorphisms have low penetrance, monozygotic twin studies suggest a low concordance rate, and increasing worldwide IBD incidence leave gaps in our understanding of IBD heritability and highlight the importance of environmental influences. Operating at the interface between environment and heritable molecular and cellular phenotypes, microRNAs (miRNAs) are a class of endogenous, small noncoding RNAs that regulate gene expression. Studies to date have identified unique miRNA expression profile signatures in IBD and preliminary functional analyses associate these deregulated miRNAs to canonical pathways associated with IBD pathogenesis. In this review, we summarize and discuss the miRNA expression signatures associated with IBD in tissue and peripheral blood, highlight miRNAs with potential future clinical applications as diagnostic and therapeutic targets, and provide an outlook on how to develop miRNA based therapies.

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“…Chen et al [31] identified NOD2 as a target of miR-122. Overexpression of miR-122 in LPSstimulated HT-29 cells inhibited LPS-induced apoptosis and down-regulated LPS-induced NOD2 expression.…”

Section: Pathwaymentioning

confidence: 99%

Implication of miRNAs for inflammatory bowel disease treatment: Systematic review

Chen¹,

Ren²,

Shi³

2014

WJGP

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Inflammatory bowel disease (IBD) is believed to develop via a complex interaction between genetic, environmental factors and the mucosal immune system. Crohn's disease and ulcerative colitis are two major clinical forms of IBD. MicroRNAs (miRNAs) are a class of small, endogenous, noncoding RNA molecules, and evolutionary conserved in animals and plants. It controls protein production at the post-transcriptional level by targeting mRNAs for translational repression or degradation. MiRNAs are important in many biological processes, such as signal transduction, cellular proliferation, differentiation and apoptosis. Considerable attention has been paid on the key role of miRNAs in autoimmune and inflammatory disease, especially IBD. Recent studies have identified altered miRNA profiles in ulcerative colitis, Crohn's disease and inflammatory bowel diseaseassociated colorectal cancer. In addition, emerging data have implicated that special miRNAs which suppress functional targets play a critical role in regulating key pathogenic mechanism in IBD. MiRNAs were found involving in regulation of nuclear transcription factor kappa B pathway (e.g. , miR-146a, miR-146b, miR-122, miR-132, miR-126), intestinal epithelial barrier function (e.g. , miR-21, miR-150, miR-200b) and the autophagic activity (e.g. , miR-30c, miR-130a, miR-106b, miR-93, miR-196). This review aims at discussing recent advances in our understanding of miRNAs in IBD pathogenesis, their role as disease biomarkers, and perspective for future investigation and clinical application. Key words: Crohn's disease; Inflammatory bowel disease; MicroRNA; Treatment; Ulcerative colitis; Biomarker Core tip: MicroRNAs (miRNAs) are a class of small, noncoding RNA molecules that post-transcriptionally regulate gene and protein expression. Recent studies have identified altered miRNA profiles in inflammatory bowel disease (IBD). Special miRNAs which suppress functional targets have been found to play a critical role in regulating key pathogenic mechanism in IBD. In this review, we discuss the possibility to use miRNAs as biomarkers and therapeutic target in IBD.Chen WX, Ren LH, Shi RH. Implication of miRNAs for inflammatory bowel disease treatment: Systematic review. World

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miR-122 targets NOD2 to decrease intestinal epithelial cell injury in Crohn’s disease

Cited by 85 publications

References 29 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

The emerging role of miRNAs in inflammatory bowel disease: a review

Implication of miRNAs for inflammatory bowel disease treatment: Systematic review

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