Long non-coding RNA expression profile in minor salivary gland of primary Sjögren’s syndrome

Shi, Huan; Cao, Ningning; Pu, Yiping; Xie, Linka; Zheng, Lingyan; Yu, Chuangqi

doi:10.1186/s13075-016-1005-2

Cited by 61 publications

(47 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LncRNAs are implicated in the pathogenesis of SS [21,22]. Particularly, a robust up-regulation of Mirt2 has been observed in myocardial infarction and correlates with the expression of multiple genes which are highly implicated in the inflammation-associated pathways, for instance, cytokine-cytokine receptor, chemokine and toll-like receptor cascades [6].…”

Section: Discussionmentioning

confidence: 99%

“…Of note, Mirt2 overexpression exerted a protective effect against IFN-c-caused inflammatory damages while Mirt2 silence exhibited a proinflammatory role in IFN-c-treated SGECs. Additionally, a study revealed that many novel lncRNA transcripts that play vital roles in the pathogenesis were dys-regulated in SS [22]. However, the potential mechanism is still not completely understood.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Xin

Liang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

Background: The interaction of long non-coding RNAs (lncRNAs)-microRNAs (miRs) exerts crucial functions in mediating inflammatory reaction. It is still unclear whether myocardial infarction associated transcript 2 (Mirt2)-miR-377 mediates the inflammatory pathogenesis in Sj€ ogren's syndrome (SS). Methods: The inflammatory lesion model was established by stimulating salivary gland epithelial cells (SGECs) by interferon gamma (IFN-c). Mirt2-and/or miR-377-transfected SGECs, as well as their negative controls, were applied to investigate the biological functions in inflammation. Cell viability and apoptosis were examined using commercial kits. Western blot was applied to quantify protein level, and enzyme-linked immuno sorbent assay (ELISA) was used to value the secretion of cytokines. Results: The up-regulation of Mirt2 was observed in IFN-c-treated SGECs. Mirt2 overexpression restored the expression of miR-377 which was repressed by IFN-c. However, miR-377 silence abolished the protective effect on cell viability, inhibitory effect on apoptosis and prohibitive role in pro-inflammatory factors. Mirt2 diminished the phosphorylated expression of crucial regulators while miR-377 silence restored the phosphorylation in IFN-c-treated SGECs. Conclusion: Mirt2 was elevated in IFN-c-treated SGECs and then up-regulated miR-377 in response to inflammatory lesions. Mechanically, in synergy with miR-377 Mirt2 blocked IFN-c-evoked activation of NF-jB and JAK/STAT signalling pathway. ARTICLE HISTORY

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Xin

Liang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

show abstract

“…Similar to other autoimmune disease, pSS patients also had a variety of autoantigens (mainly SSA and SSB antigen), which could be presented to the T cells or be recognized by B cells to trigger the release of autoantibodies to promote disease progression (22,23), and this attached importance to the enrichment function of antigen presentation. This important function was also reported in a previous study on LncRNAs analysis in the minor salivary glands of pSS patients (24), and some immune-related signaling pathways like NF-κB signaling pathway, TNF signaling pathway, and natural killer cell Eleven selected LncRNAs were involved in the RT-qPCR validation stage. Among them, LINC00426, TPTEP1-202, CYTOR, NRIR, and BISPR were found to be aberrantly expressed.…”

Section: Discussionsupporting

confidence: 79%

LncRNA and mRNA expression profile of peripheral blood mononuclear cells in primary Sjögren’s syndrome patients

Luo

Chen

et al. 2019

Preprint

View full text Add to dashboard Cite

Background The aim of this study was to elucidate the expression profile and the potential role of long non-coding RNA (LncRNA) in the peripheral blood mononuclear cells of primary Sjögren’s syndrome (pSS) patients. Methods RNA-seq technology was used to detect the differentially expressed LncRNAs and mRNAs between five paired pSS patients and healthy control PBMCs. The selected LncRNAs were detected in the validation study by RT-qPCR in 16 paired pSS patients and healthy controls. The GO, KEGG, co-localization, and co-expression analysis were performed to enrich the potential gene functions and pathways.Results In this study, 44 out of 1772 LncRNAs and 1034 out of 15424 mRNAs were expressed differentially in the PBMCs of pSS patients. LINC00426, TPTEP1-202, CYTOR, NRIR, and BISPR were validated as aberrantly expressed, and these LncRNAs strongly correlated with disease activity of pSS. GO and KEGG pathway analysis revealed the significant enrichment of biological processes, cellular components, and molecular function of the up and down-regulated mRNAs, which were mainly concentrated in the immune response and immune system processes. Co-localization and co-expression analysis also revealed that differentially expressed LncRNAs in the PBMCs of pSS were strongly correlated to the mRNA functioning associated with immune response and cell metastasis. Conclusions Numerous LncRNAs and mRNAs were found differentially expressed in the PBMCs of pSS patients, especially NRIR and BISPR; they interacted with the co-localized and co-expressed mRNAs, which might participate in the pathogenesis of pSS through the NF-κB, JAK-STAT, and other signaling pathways that regulate cell metastasis.

show abstract

“…This study identified more than 1000 lncRNAs that were differentially expressed in pSS salivary tissue. Of note, expression of specific lncRNAs showed strong correlations with SS disease manifestations including the presence of rheumatoid factor (RF), anti-La (SSB) autoantibodies, immunoglobulin (Ig) A, and IgM titers [130], suggesting a pathogenic role for certain lncRNAs in disease.…”

Section: Mechanisms Of Innate Immune Activation In Ssmentioning

confidence: 99%

Innate immunity in Sjögren's syndrome

Kiripolsky

McCabe

Kramer

2017

Clinical Immunology

View full text Add to dashboard Cite

Sjögren’s syndrome (SS) is an autoimmune disease of exocrine tissue that primarily affects women. Although patients typically experience xerostomia and xerophthalmia, numerous systemic disease manifestations are seen. Innate immune hyperactivity is integral to many autoimmune diseases, including SS. Results from SS mouse models suggest that innate immune dysregulation drives disease and this is a seminal event in SS pathogenesis. Findings in SS patients corroborate those in mouse models, as innate immune cells and pathways are dysregulated both in exocrine tissue and in peripheral blood. We will review the role of the innate immune system in SS pathogenesis. We will discuss the etiology of SS with an emphasis on innate immune dysfunction. Moreover, we will review the innate cells that mediate inflammation in SS, the pathways implicated in disease, and the potential mechanisms governing their dysregulation. Finally, we will discuss emerging therapeutic approaches to target dysregulated innate immune signaling in SS.

show abstract

Long non-coding RNA expression profile in minor salivary gland of primary Sjögren’s syndrome

Cited by 61 publications

References 42 publications

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

LncRNA and mRNA expression profile of peripheral blood mononuclear cells in primary Sjögren’s syndrome patients

Innate immunity in Sjögren's syndrome

Contact Info

Product

Resources

About