Human and Viral microRNA Expression in Sjögren Syndrome

Cotrim, Ana P.; Alevizos, Ilias

doi:10.3899/jrheum.141068

Cited by 4 publications

(3 citation statements)

References 16 publications

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“…Despite these limitations, our study may have several points of strength. First, our experiments are consistent with previous studies on miRNome profiling in pSS 45,46 . We substantiated previous findings on the deregulation of a large number of microRNA in pSS MSGB 10,13,45 .…”

Section: (Available With the Online Version Of This Article)supporting

confidence: 92%

MicroRNA-mediated Regulation of Mucin-type O-glycosylation Pathway: A Putative Mechanism of Salivary Gland Dysfunction in Sjögren Syndrome

et al. 2019

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Objective.To investigate microRNA (miRNA) that is potentially implicated in primary Sjögren syndrome (pSS)–related salivary hypofunction in labial salivary glands and to study miRNA-mediated mechanisms underlying oral dryness and altered rheology, focusing on the mucin O-glycosylation pathway.Methods.We performed miRNA expression profiling in minor salivary gland samples of patients with pSS presenting a different impairment in their unstimulated salivary flow rate. A computational in silico analysis was performed to identify genes and pathways that might be modulated by the deregulated miRNA that we had identified. To confirm in silico analysis, expression levels of genes encoding for glycosyltransferases and glycan-processing enzymes were investigated using Human Glycosylation-RT2 Profiler PCR Array.Results.Among 754 miRNA analyzed, we identified 126 miRNA that were significantly deregulated in pSS compared to controls, with a trend that was inversely proportional with the impairment of salivary flow rates. An in silico approach pinpointed that several upregulated miRNA in patients with pSS target important genes in the mucin O-glycosylation. We confirmed this prediction by quantitative real-time PCR, highlighting the downregulation of some glycosyltransferase and glycosidase genes in pSS samples compared to controls, such as GALNT1, responsible for mucin-7 glycosylation.Conclusion.Collectively, our data suggest that the expression of different predicted miRNA-target genes in the mucin type O-glycan biosynthesis pathway is altered in pSS patients with low salivary flow and that the miRNA expression profile could influence the glycosidase expression levels and consequently the rheology in pSS.

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Section: (Available With the Online Version Of This Article)supporting

confidence: 92%

MicroRNA-mediated Regulation of Mucin-type O-glycosylation Pathway: A Putative Mechanism of Salivary Gland Dysfunction in Sjögren Syndrome

et al. 2019

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“…The disease primarily affects middle-aged females. However, establishing the diagnosis of SS is often challenging, since the symptoms are nonspecific, while no single laboratory test allows for a definitive diagnosis and there are no disease-specific diagnostic criteria (2). Although the exact pathogenic mechanisms are not yet fully elucidated, immune system abnormalities are considered to be important in SS pathogenesis, including hypergammaglobulinemia, increased levels of autoantibodies against Ro/SS-associated antigen A (Ro/SSA) and La/SS-associated antigen B (La/SSB) (3), and exocrine gland histology characterized by focal lymphocyte infiltrates surrounding the glandular ducts (4,5).…”

Section: Introductionmentioning

confidence: 99%

Decreased microRNA-181a and -16 expression levels in the labial salivary glands of Sjï¿½gren syndrome patients

Wang

Zhang

et al. 2017

Exp Ther Med

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Abstract. Sjögren syndrome (SS) is characterized by dysfunction of the exocrine glands, particularly the salivary and lacrimal glands. Thus, labial salivary gland biopsy is useful method for diagnosing SS. The aim of the present study was to investigate the microRNA (miRNA or miR) profile of labial salivary glands obtained from SS patients and to examine the correlation of miR-181a and -16 levels with the pathological grade in SS. miRNA expression in labial salivary gland tissues was profiled in 3 female patients with primary SS and 3 female patients with non-SS sicca syndrome using microarray analysis. In addition, a literature search and miRNA target gene prediction were performed to collect miRNAs involved in SS pathogenesis. Subsequent to integrating all database results, miR-181a and -16 were identified to be associated with the Ro/SS-associated antigen A and La/SS-associated antigen B during SS pathogenesis. Therefore, these miRNAs were selected for further verification in labial salivary gland tissues of 28 patients with SS and 18 non-SS sicca syndrome control individuals by quantitative reverse transcription-quantitative polymerase chain reaction. Compared with the control group, 76 miRNAs were upregulated and 51 were downregulated in the labial salivary gland of SS patients according to microarray results. In particular, miR-181a and -16 expression levels in the labial salivary gland of SS patients were decreased in comparison with those in the controls. Furthermore, the decreased expression levels of these miRNAs were associated with the labial salivary pathological focus scores. In conclusion, the present study examined the miRNA profiles in the labial salivary glands of SS patients and detected decreased miR-181a and -16 expression levels compared with the control individuals. Finally, the decreased levels of miR-181a and -16 were associated with the salivary gland pathological focus scores, suggesting that miR-181a and -16 may serve a role in the pathogenesis of SS.

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“…Floch et al have demonstrated in a gastric MALT lymphoma mouse model that chronic Helicobacter pylori infection may induce the overexpression of micro-RNAs 21a, 135b, 142a, 150, and 155, which prevents the transcription of the gene coding for the proapoptotic protein tumor protein P53-inducible nuclear protein 1 (TP53INP1) [52]. Some of these micro-RNAs control the production of antibodies (including autoantibodies) [53], and others may belong to viruses infecting host cells as in the case of EBV infection [54]. Viral micro-RNAs such as EBV micro-RNA 181a may be overexpressed in infected cells and favour cell survival and proliferation, thus paving the way for the development of proliferative disease.…”

Section: Resultsmentioning

confidence: 99%

Microbial Agents as Putative Inducers of B Cell Lymphoma in Sjögren’s Syndrome through an Impaired Epigenetic Control: The State-of-The-Art

Talotta

Sarzi‐Puttini

Atzeni

2019

Journal of Immunology Research

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Introduction Understanding the mechanisms underlying the pathogenesis of Sjögren's syndrome (SS) is crucially important in order to be able to discriminate the steps that lead to B cell transformation and promptly identify the patients at risk of lymphomagenesis. The aim of this narrative review is to describe the evidence concerning the role that infections or dysbiosis plays in the epigenetic control of gene expression in SS patients and their possible involvement in B cell lymphomagenesis. Materials and Methods We searched the PubMed and Google Scholar databases and selected a total of 92 articles published during the last 25 years that describe experimental and clinical studies of the potential associations of microbiota and epigenetic aberrations with the risk of B cell lymphoma in SS patients. Results and Discussion The genetic background of SS patients is characterized by the hyperexpression of genes that are mainly involved in regulating the innate and adaptive immune responses and oncogenesis. In addition, salivary gland epithelial cells and lymphocytes both have an altered epigenetic background that enhances the activation of proinflammatory and survival pathways. Dysbiosis or chronic latent infections may tune the immune response and modify the cell epigenetic machinery in such a way as to give B lymphocytes an activated or transformed phenotype. It is also worth noting that transposable integrated retroelements may participate in the pathogenesis of SS and B cell lymphomagenesis by inducing DNA breaks, modulating cell gene expression, or generating aberrant transcripts that chronically stimulate the immune system. Conclusions Microorganisms may epigenetically modify target cells and induce their transcriptome to generate an activated or transformed phenotype. The occurrence of lymphoma in more than 15% of SS patients may be the end result of a combination of genetics, epigenetics, and dysbiosis or latent infections.

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Human and Viral microRNA Expression in Sjögren Syndrome

Cited by 4 publications

References 16 publications

MicroRNA-mediated Regulation of Mucin-type O-glycosylation Pathway: A Putative Mechanism of Salivary Gland Dysfunction in Sjögren Syndrome

MicroRNA-mediated Regulation of Mucin-type O-glycosylation Pathway: A Putative Mechanism of Salivary Gland Dysfunction in Sjögren Syndrome

Decreased microRNA-181a and -16 expression levels in the labial salivary glands of Sjï¿½gren syndrome patients

Microbial Agents as Putative Inducers of B Cell Lymphoma in Sjögren’s Syndrome through an Impaired Epigenetic Control: The State-of-The-Art

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