• Animals
• Mice
• Male
• Nod2 Signaling Adaptor Protein/metabolism
• Nod2 Signaling Adaptor Protein/genetics
• Nerve Tissue Proteins/metabolism
• Nerve Tissue Proteins/genetics
• Nerve Tissue Proteins/pharmacology
• Mice, Inbred C57BL
• Cocaine- and Amphetamine-Regulated Transcript Protein
• Receptors, G-Protein-Coupled/metabolism
• Receptors, G-Protein-Coupled/genetics
• Hyperalgesia/metabolism
• Hyperalgesia/chemically induced
• Spinal Cord Dorsal Horn/metabolism
• Spinal Cord Dorsal Horn/drug effects
• Disease Models, Animal
• Mice, Knockout

• 1R01NS113257-01 NINDS NIH HHS

• Crohn's disease
• Diagnosis
• Fibrosis
• Inflammation
• Therapy
• miRNA

• Crohn Disease/genetics
• Crohn Disease/therapy
• Crohn Disease/pathology
• MicroRNAs/genetics
• Humans
• Animals
• Inflammation/genetics
• Fibrosis/genetics

• Inflammatory bowel disease (IBD)
• MicroRNA (miRNA)
• Pathogenesis
• Therapy
• miRNA signature

• Humans
• MicroRNAs/genetics
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/therapy
• Animals

• Assiut University

• Epigenetics
• Female genitalia
• Pig
• Semen
• ncRNA

• Pregnancy
• Swine
• Female
• Male
• Animals
• Semen
• Spermatozoa/physiology
• Uterus
• Insemination, Artificial/veterinary
• MicroRNAs/genetics
• Mammals

• Crohn’s disease
• autophagy
• colitis
• fibrosis
• inflammatory bowel disease
• intestinal fibrosis

• Ministerio de Ciencia e Innovación
• Instituto de Salud Carlos III

• IBD
• microRNAs

• Maladies Inflammatoires Chroniques Intestinales en Lorraine
• Centre Hospitalier Régional Universitaire

• inflammatory bowel disease
• intestinal fibrosis
• miRNAs
• therapeutic target

• Colitis, ulcerative
• Crohn disease
• Fibrosis
• Inflammatory bowel disease

• biomarker
• cancer
• expression
• mir-671
• prognostic

• T cells
• gut homeostasis
• inflammatory bowel disease (IBD)
• innate immunity
• intestinal epithelial cells (IECs)
• miRNA
• microbiota

• Humans
• MicroRNAs/genetics
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/therapy
• Dysbiosis
• Homeostasis
• Chronic Disease

• R01 AI127853 NIAID NIH HHS
• R01 AI151953 NIAID NIH HHS
• R01 CA267479 NCI NIH HHS
• R21 AI174047 NIAID NIH HHS

• Intestinal epitheliums regeneration
• Intestinal inflammation
• NF-κB
• miR-146a-5p

• Swine
• Animals
• Mice
• Lipopolysaccharides/toxicity
• Lipopolysaccharides/metabolism
• NF-kappa B/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Signal Transduction
• Inflammation/genetics
• Anti-Inflammatory Agents
• Epithelium/metabolism

Inflammatory bowel diseases are considered immune disorders with a complex genetic architecture involving constantly changing endogenous and exogenous factors. The rapid evolution of genomic technologies and the emergence of newly discovered molecular actors are compelling the research community to reevaluate the knowledge and molecular processes. The human intestinal tract contains intestinal human microbiota consisting of commensal, pathogenic, and symbiotic strains leading to immune responses that can contribute and lead to both systemic and intestinal disorders including IBD. In this review, we attempted to highlight some updates of the new IBD features related to genomics, microbiota, new emerging therapies and some major established IBD risk factors.

• study received no specific funding

• Crohn’s disease
• colitis-associated cancer
• extraintestinal manifestations
• non-coding RNA
• ulcerative colitis

• R01 HL124078 NHLBI NIH HHS
• R01 HL133022 NHLBI NIH HHS

It has been reported that the traditional Chinese medicine Huangqin-Tang decoction (HQT) has a protective effect on the epithelial barrier function of ulcerative colitis, but its mechanism has not been fully clarified. This study intends to explore the protective mechanism of HQT in regulating microRNA (miRNA) for the first time.

Based on the Balb/c mice ulcerative colitis model, the mice were given a gavage of 0.1 mL/10 g HQT every day for 7 days; on the 8th day, the colon of the mice was dissected, the length of the colon for the mice was measured, and the score was given based on this. Analysis of colonic mucosal injury was conducted by hematoxylin-eosin staining. Then, the differential miRNA was screened and sequenced in colon tissue using the HiSeq platform. And the differential miR-185-3p gene was verified by RT-PCR. Finally, the effects of HQT on miR-185-3p, occludin protein expression, and transepithelial electrical resistance (TEER) value were observed in combination with the CaCo₂ intestinal epithelial cell model.

HQT treatment can alleviate the shortening of colon length and reverse the intestinal mucosal injury. miRNA sequencing of colonic tissue showed that miR-185-3p was significantly downregulated in the model group, while HQT could upregulate miR-185-3p, thereby affecting the myosin light chain kinase (MLCK)/myosin light chain phosphorylation (p-MLC) pathway and leading to increased expression of occludin protein, which ultimately protected the intestinal epithelial barrier function.

HQT can protect colon epithelial barrier function by regulating miR-185-3p.

• Micro RNA
• genetic predisposition
• intestinal inflammation.
• necrotizing enterocolitis
• neonates
• spontaneous intestinal perforation

• Biomarker
• Domestic animals
• Pathology
• Reproduction
• miRNA

Research on inflammatory bowel disease (IBD) has produced mounting evidence for the modulation of microRNAs (miRNAs) during pathogenesis. MiRNAs are small, non-coding RNAs that interfere with the translation of mRNAs. Their high stability in free circulation at various regions of the body allows researchers to utilise miRNAs as biomarkers and as a focus for potential treatments of IBD. Yet, their distinct regulatory roles at the gut epithelial barrier remain elusive due to the fact that there are several external and cellular factors contributing to gut permeability. This review focuses on how miRNAs may compromise two components of the gut epithelium that together form the initial physical barrier: the mucus layer and the intercellular epithelial junctions. Here, we summarise the impact of miRNAs on goblet cell secretion and mucin structure, along with the proper function of various junctional proteins involved in paracellular transport, cell adhesion and communication. Knowledge of how this elaborate network of cells at the gut epithelial barrier becomes compromised as a result of dysregulated miRNA expression, thereby contributing to the development of IBD, will support the generation of miRNA-associated biomarker panels and therapeutic strategies that detect and ameliorate gut permeability.

• gut epithelial barrier
• inflammatory bowel disease
• intercellular junctions
• microRNAs
• mucus layer

• Cancer
• Colorectal cancer
• Crohn's disease
• Diagnosis
• Inflammatory bowel disease
• MicroRNA
• Prognosis
• Targets
• Ulcerative colitis

• Crohn’s disease (CD)
• IBD
• collaborative cross
• diversity outbred
• extracellular vesicles
• genetic diversity
• humanized mice
• miRNA
• ulcerative colitis (UC)

• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/immunology
• Colitis, Ulcerative/pathology
• Databases, Genetic
• Decision Trees
• Disease Progression
• Gene Expression Regulation
• Gene Ontology
• Gene Regulatory Networks
• Humans
• Inflammation/genetics
• MicroRNAs/genetics
• MicroRNAs/metabolism
• RNA/genetics
• RNA/metabolism
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Severity of Illness Index

• NOD2 gene
• Single nucleotide polymorphism
• Systemic lupus erythematosus
• miRNA

• Apoptosis
• Autoimmune diseases
• Autophagy
• miRNAs

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract that mainly affects young people. IBD is associated with various gastrointestinal symptoms, and thus, affects the quality of life of patients. Currently, the pathogenesis of IBD is poorly understood. Although intestinal bacteria and host immune response are thought to be major factors in its pathogenesis, a sufficient explanation of their role in its pathophysiologic mechanism has not been presented. MicroRNAs (miRNAs), which are small RNA molecules that regulate gene expression, have gained attention as they are known to participate in the molecular interactions of IBD. Recent studies have confirmed the important role of miRNAs in targeting certain molecules in signaling pathways that regulate the homeostasis of the intestinal barrier, inflammatory reactions, and autophagy of the intestinal epithelium. Several studies have identified the specific miRNAs associated with IBD from colon tissues or serum samples of IBD patients and have attempted to use them as useful diagnostic biomarkers. Furthermore, some studies have attempted to treat IBD through intracolonic administration of specific miRNAs in the form of nanoparticle. This review summarizes the latest findings on the role of miRNAs in the pathogenesis, diagnosis, and treatment of IBD.

• Crohn's disease
• inflammatory bowel diseases
• microRNAs
• ulcerative colitis

It has been shown that miR-192 is abnormally expressed in a variety of cancer types and participates in different kinds of signaling pathways. The role of miR-192 in the diagnosis and prognosis of cancer has not been verified. This article is aimed at exploring the diagnostic and prognostic value of miR-192 through a systematic review and meta-analysis.

A systematic search was performed through PubMed, Embase, Web of Science, and Cochrane Library databases up to June 16, 2020. A total of 16 studies were enrolled in the meta-analyses, of which 11 articles were used for diagnostic meta-analysis and 5 articles were used for prognostic meta-analysis. The values of sensitivity and specificity using miR-192 expression as a diagnostic tool were pooled in the diagnostic meta-analysis. The hazard ratios (HRs) of overall survival (OS) with 95 confidence intervals (CIs) were extracted from the studies, and pooled HRs were evaluated in the prognostic meta-analysis. Eleven studies including 667 cancer patients and 514 controls met the eligibility criteria for the diagnostic meta-analysis. Five studies including 166 patients with high miR-192 expression and 236 patients with low miR-192 expression met the eligibility criteria for the prognostic meta-analysis.

The overall diagnostic accuracy was as follows: sensitivity 0.79 (95%CI = 0.75-0.82), specificity 0.74 (95%CI = 0.64-0.82), positive likelihood ratio 3.03 (95%CI = 2.11-4.34), negative likelihood ratio 0.29 (95%CI = 0.23-0.37), diagnostic odds ratio 10.50 (95%CI = 5.89-18.73), and area under the curve ratio (AUC) 0.82 (95%CI = 0.78-0.85). The overall prognostic analysis showed that high expression of miR-192 in patients was associated with positive survival (HR = 0.62, 95%CI : 0.41-0.93, p = 0.020).

Our results revealed that miR-192 was a potential biomarker with good sensitivity and specificity in cancers. Moreover, highly expressed miR-192 predicted a good prognosis for patients.

• Miichthys miiuy
• NF-κB
• NOD1
• microRNA
• negative regulation

• Biomarker
• Dog
• Inflammatory bowel disease
• microRNAs

• Animals
• Biomarkers/blood
• Colon/metabolism
• Dog Diseases/blood
• Dog Diseases/genetics
• Dog Diseases/metabolism
• Dog Diseases/pathology
• Dogs
• Female
• Gene Expression Profiling/veterinary
• Inflammatory Bowel Diseases/blood
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/veterinary
• Intestinal Mucosa/metabolism
• Male
• MicroRNAs/genetics
• MicroRNAs/metabolism

Increasing evidence suggest the significance of inflammation in the progression of cancer, for example the development of colorectal cancer in Inflammatory Bowel Disease (IBD) patients. Long-lasting inflammation in the gastrointestinal tract causes serious systemic complications and breaks the homeostasis of the intestine, where the altered expression of regulatory genes and miRNAs trigger malignant transformations. Several steps lead from acute inflammation to malignancies: epithelial-to-mesenchymal transition (EMT) and inhibitory microRNAs (miRNAs) are known factors during multistage carcinogenesis and IBD pathogenesis. In this review, we outline the interactions between EMT components and miRNAs that may affect cancer development during IBD.

• Inflammatory Bowel Disease (IBD)
• epithelial-to-mesenchymal transition (EMT)
• microRNAs

MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by suppressing the target mRNA and inhibiting translation in order to regulate multiple biological processes. miRNAs play important roles as oncogenes or tumor suppressors in the development of various types of human cancer. The regulation of mammalian target of rapamycin (mTOR) by miRNAs has been studied in several types of cancer, including colorectal cancer (CRC). However, to the best of our knowledge, only limited information regarding the function of miRNAs in human CRC is available. In the present study, the expression of 22 miRNAs in CRC cell lines were investigated in regard to key genes in the mTOR pathway. Initially, it was revealed that mTOR, regulatory-associated protein of mTOR complex I and rapamycin-intensive companion of mTOR were overexpressed in CRC cell lines when compared with a normal colorectal cell line. Subsequently, putative miRNA-mRNA associations were identified via multiple miRNA target prediction programs. The expression levels for the candidate miRNAs were validated using quantitative real-time polymerase chain reaction. Expression analysis revealed that, among 20 miRNAs, five miRNAs (miR-496, miR-1185, miR-654, miR-3183 and miR-495) exhibited significant downregulation in association with the mTOR signaling pathway. Taken together, the results from the present study suggest that several miRNAs that are associated with CRC, with possible roles in mTOR signaling, may have potential therapeutic or diagnostic benefits in CRC treatment.

• colorectal cancer
• mammalian target of rapamycin
• microRNA
• rapamycin-insensitive companion of mammalian target of rapamycin
• regulatory-associated protein of mammalian target of rapamycin complex 1

• CAC
• CRC
• IBD
• miR-19a
• miR-21
• miR-31
• miRNAs

• Crohn's disease
• bioinformatics
• colorectal cancer
• microRNA (miR)-192/215-5p

• colorectal cancer (CRC)
• competing endogenous RNAs (ceRNA)
• lncRNA Urothelial Cancer Associated 1 (UCA1)
• long non-coding RNA (lncRNA)

• NA Institut National de la Santé et de la Recherche Médicale
• NA Centre National de la Recherche Scientifique
• R17037EE - RAB17005EEA Comité du Nord de la Ligue Nationale contre le Cancer

• apoptosis
• autophagy
• inflammation
• inflammatory bowel disease
• microRNA

• inflammatory bowel disease
• immunoregulation
• cytokine
• ulcerative colitis
• crohn’s disease
• treatment

Accumulating evidence demonstrates that microRNA- (miR-) mediated posttranscriptional regulation plays an important role in autophagy in inflammatory bowel disease (IBD), a disease that is difficult to manage clinically because of the associated chronic recurrent nonspecific inflammation. Research indicates that microRNAs regulate autophagy via different pathways, playing an important role in the IBD process and providing a new perspective for IBD research. Related studies have shown that miR-142-3p, miR-320, miR-192, and miR-122 target NOD2, an IBD-relevant autophagy gene, to modulate autophagy in IBD. miR-142-3p, miR-93, miR-106B, miR-30C, miR-130a, miR-346, and miR-20a regulate autophagy by targeting ATG16L1 through several different pathways. miR-196 can downregulate IRGM and suppress autophagy by inhibiting the accumulation of LC3II. During the endoplasmic reticulum stress response, miR-665, miR-375, and miR-150 modulate autophagy by regulating the unfolded protein response, which may play an important role in IBD intestinal fibrosis. Regarding autophagy-related pathways, miR-146b, miR-221-5p, miR-132, miR-223, miR-155, and miR-21 regulate NF-κB or mTOR signaling to induce or inhibit autophagy in intestinal cells by releasing anti- or proinflammatory factors, respectively.

Background: Given the overlap of clinical manifestations and pathological characteristics between Parkinson's disease (PD) and multiple system atrophy (MSA), we investigated the associations between five functional polymorphisms of nucleotide-binding oligomerization domain protein 2 (NOD2) which were associated with PD, and MSA in a Chinese population.

Methods: A cohort of 431 MSA patients and 441 unrelated healthy controls (HCs) were included in the study. Five polymorphisms in NOD2, including P268S, R702W, G908R, 1007fs, and rs3135500, were genotyped. The mRNA expression of NOD2 in peripheral mononuclear cells (PBMCs) in 32 MSA patients were analyzed using RT-PCR, and the concentration of NOD2 and α-synuclein from plasma of 57 MSA patients were also measured by ELISA analysis.

Results: No heterozygous or homozygous for R702W, G908R, and 1007fs were found in all the subjects. For rs3135500, differences in genotype distributions, dominant and additive genetic models, were found between MSA and HCs, and between MSA Parkinsonism (MSA-P) patients and HCs. Interestingly, patients carrying the “A” allele of rs3135500 had higher mRNA NOD2 level from PBMCs and NOD2 protein from plasma than patients without this allele (p = 0.028 and p = 0.036, respectively). In addition, we also found the concentration of NOD2 in plasma was positively correlated with the levels of NOD2 mRNA in PBMC and α-synuclein in plasma (R = 0.761 and 0.832, respectively).

Conclusion: Our findings suggest that the rs3135500 variant in the NOD2 gene might increase the risk for MSA and might provide new evidence that inflammation mediated by NOD2 involved in the pathogenesis of MSA. Further association studies involving a larger number of participants, as well as functional studies, are needed to confirm our current findings.

• NOD2
• association
• expression
• mRNA
• multiple system atrophy
• variants
• α-synuclein

Localized cutaneous leishmaniasis (LCL) is a chronic disease characterized by ulcerated skin lesion(s) and uncontrolled inflammation. The mechanisms underlying the pathogenesis of LCL are not completely understood, and little is known about posttranscriptional regulation during LCL. MicroRNAs (miRNAs) are non-coding small RNAs that regulate gene expression and can be implicated in the pathogenesis of LCL. We investigated the involvement of miRNAs and their targets genes in human LCL using publicly available transcriptome data sets followed by ex vivo validation. Initial analysis highlighted that miRNA expression is altered during LCL, as patients clustered separately from controls. Joint analysis identified eight high confidence miRNAs that had altered expression (−1.5 ≤ fold change ≥ 1.5; p < 0.05) between cutaneous ulcers and uninfected skin. We found that the expression of miR-193b and miR-671 are greatly associated with their target genes, CD40 and TNFR, indicating the important role of these miRNAs in the expression of genes related to the inflammatory response observed in LCL. In addition, network analysis revealed that miR-193b, miR-671, and TREM1 correlate only in patients who show faster wound healing (up to 59 days) and not in patients who require longer cure times (more than 60 days). Given that these miRNAs are associated with control of inflammation and healing time, our findings reveal that they might influence the pathogenesis and prognosis of LCL.

• Leishmania braziliensis
• TREM-1
• human leishmaniasis
• microRNA
• skin
• transcriptome

• ER stress
• autophagy
• extraintestinal disease
• inflammatory bowel disease
• innate immunity
• intestinal homeostasis

• Intestinal mucosal barrier
• JAK/STAT3 signaling pathway
• MircoRNA-495
• STAT3
• Ulcerative colitis

• Animals
• Antagomirs/metabolism
• Apoptosis/physiology
• Cell Differentiation/physiology
• Cell Line, Tumor
• Colitis, Ulcerative/genetics
• Disease Models, Animal
• Mice, Inbred BALB C
• MicroRNAs/genetics
• STAT3 Transcription Factor/metabolism
• Signal Transduction/physiology

• Crohn’s disease
• differential expression analysis
• mRNA
• microRNA
• microRNA–mRNA co-expression

• Computational Biology/methods
• Crohn Disease/genetics
• Gene Expression Profiling
• Gene Expression Regulation
• Gene Regulatory Networks
• Humans
• Inflammatory Bowel Diseases/genetics
• Intestinal Mucosa/metabolism
• Intestinal Mucosa/pathology
• MicroRNAs/genetics
• RNA Interference
• RNA, Messenger/genetics
• Transcriptome

• COX2
• Cannabis
• MMP9
• THCA
• cannabinoid receptors
• inflammatory bowel disease

• Autophagy
• Diagnosis
• Immune homeostasis
• Inflammatory bowel diseases
• Intestinal epithelial barrier
• MiRNA

• Autophagy
• Biomarkers/metabolism
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/metabolism
• Diagnosis, Differential
• Epithelial Cells/physiology
• Homeostasis/genetics
• Homeostasis/immunology
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/metabolism
• Intestinal Mucosa/immunology
• Intestinal Mucosa/physiopathology
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Molecular Targeted Therapy
• Severity of Illness Index