Immune-related miRNA expression patterns in peripheral blood mononuclear cells differ in multiple sclerosis relapse and remission

Baulina, Natalia; Кулакова, О. Г.; Kiselev, Ivan; Osmak, German; Popova, E. V.; Boyko, A. N.; Фаворова, О. О.

doi:10.1016/j.jneuroim.2018.01.005

Cited by 50 publications

(41 citation statements)

References 62 publications

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“…Because exosomes were shown to contribute to intercellular communication by transporting signals into the target cells either close to or distant from the cells of exosome origin [12,16], we investigated the effect of RA-exosomes on Treg differentiation and found that RA-exosomes could inhibit Treg differentiation in vitro. Because miRNA has been shown to play an important role in the differentiation and function of immune cells [18][19][20][21][22][23], we next analyzed miRNA expression profiles in RA-exosomes as compared with those in HC-exosomes by microarray analysis. The results showed remarkable differences in miRNA profiles between RA-exosomes and HC-exosomes.…”

Section: Discussionmentioning

confidence: 99%

Circulating Exosomal miR-17 Inhibits the Induction of Regulatory T Cells via Suppressing TGFBR II Expression in Rheumatoid Arthritis

Wang

Jia

et al. 2018

Cell Physiol Biochem

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Background/Aims: A reduced prevalence of circulating regulatory T cells (Tregs)is a hallmark of inflammatory rheumatoid arthritis (RA). However, the underlying mechanisms of alterations of Tregs are unclear. Methods: The ratio of Tregs in peripheral blood of healthy controls (HCs) and patients with RA was determined by flow cytometry. MicroRNA (miRNA) expression profiles in exosomes derived from RA patients (RA-exosomes) and in those from HCs (HC-exosomes) were detected by microarray analysis, and miR-17 was measured by quantitative real-time PCR. Transforming growth factor beta receptor II (TGFBR II) expressed by T cells was measured by flow cytometry. The interaction between miR-17 and TGFBR II was evaluated by dual-luciferase reporter assay. Results: We found that RA-exosomes can selectively affect Treg differentiation in vitro. Several miRNAs are more abundant in the RA-exosomes than in HC-exosomes. Among those upregulated in patients with RA, miR-17 can suppress Treg induction by inhibiting the expression of TGFBR II. Conclusion: Our findings imply that altered miRNA expression in RA-exosomes may contribute to the pathogenesis of RA by disrupting the homeostasis of Tregs.

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Section: Discussionmentioning

confidence: 99%

Circulating Exosomal miR-17 Inhibits the Induction of Regulatory T Cells via Suppressing TGFBR II Expression in Rheumatoid Arthritis

Wang

Jia

et al. 2018

Cell Physiol Biochem

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“…[160][161][162][163]168 Also, cigarette smoking could downregulate miR-21-5p in SPMS, more specifically in the relapse phases (Tables 1 and 2). 115,139,193 This miRNA could target numerous MS risk genes, including SLC2A4RG, MALT1, STAT3, TAGAP, DDAH1, and IL12A, as indicated by the GWS and IMSGC studies (Table 3). [160][161][162][163]166,167 Notably, maternal tobacco smoking could induce miR-223 upregulation in the blood, which subsequently affected Treg counts and functionality (Table 1).…”

Section: Data Extractionmentioning

confidence: 96%

“…[160][161][162][163] miR-126 was recently found to be significantly upregulated in RRMS cases. 139,242 miR-181c could promote Th17 differentiation, induce autoimmunity, and mediate EAE and was upregulated in the peripheral blood and the CSF of MS patients. 22,159,243 Furthermore, cigarette smoking could cause a global decrease in miRNAs profiles in alveolar MØ.…”

Section: Data Extractionmentioning

confidence: 99%

Environmental Influencers, MicroRNA, and Multiple Sclerosis

Mohammed

2020

J Cent Nerv Syst Dis

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Multiple sclerosis (MS) is a complex neurological disorder characterized by an aberrant immune system that affects patients’ quality of life. Several environmental factors have previously been proposed to associate with MS pathophysiology, including vitamin D deficiency, Epstein-Barr virus (EBV) infection, and cigarette smoking. These factors may influence cellular molecularity, interfering with cellular proliferation, differentiation, and apoptosis. This review argues that small noncoding RNA named microRNA (miRNA) influences these factors’ mode of action. Dysregulation in the miRNAs network may deeply impact cellular hemostasis, thereby possibly resulting in MS pathogenicity. This article represents a literature review and an author’s theory of how environmental factors may induce dysregulations in the miRNAs network, which could ultimately affect MS pathogenicity.

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“…This result confirms previous studies on the impact of miRNAs on the transcriptional network in MS pathogenesis. 23,[28][29][30][31] Our research demonstrates for the first time that the CSF profile of remitting MS (Rem) is more closely related to the profile of controls than relapsing MS (Rel) because (1) the SiPas target analysis scores were the lowest (if not absent) for the miRNAs differentially expressed between Rem vs SC (Rem/SC), whereas the scores were the highest for the ones between Rel/Rem and (2) that no common SiPas specifically stood out for the dysregulated miRNAs in Rel and Rem compared with controls. At the mRNA level, it is worth noting that, unlike most of the genes regulated by miRNAs from all groups, PLAGL2 and LMNB2 were specifically clustered to the Rel/Rem and Rem/SC subgroups.…”

Section: Csf-predominant Mirna Dysregulation and Mirna Species Newly mentioning

confidence: 99%

CSF microRNAs discriminate MS activity and share similarity to other neuroinflammatory disorders

Perdaens

Dang

D’Auria

et al. 2020

Neurol Neuroimmunol Neuroinflamm

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ObjectiveTo perform a comprehensive multicompartment analysis of microRNA (miRNA) expression in multiple sclerosis (MS) linked to disease activity and compared with other neuroinflammatory diseases through a retrospective cross-sectional study.MethodsOne hundred twenty-seven miRNAs were measured by PCR arrays on pooled CSF, serum, and peripheral blood mononuclear cell (PBMC) samples of 10 patients with relapsing MS and 10 controls. Sixty-four miRNAs were then measured by quantitative PCR on individual CSF samples of patients with relapsing or remitting MS and controls (n = 68). Fifty-seven miRNAs were analyzed in the CSF from a second cohort (n = 75), including patients with MS, neuroinfectious, or neuroinflammatory diseases and controls. MiRNAs significantly dysregulated in the CSF were analyzed on individual serum/PBMC samples (n = 59/48) of patients with relapsing or remitting MS and controls. Post hoc analysis consisted of principal component analysis (PCA), gene set, and pathway enrichment analysis.ResultsTwenty-one miRNAs were differentially expressed, mainly upregulated in the CSF during MS relapses. Relapsing MS and neuroinfectious/inflammatory diseases exhibited a partially overlapping CSF miRNA expression profile. Besides confirming the association of miR-146a-5p/150-5p/155-5p with MS, 7 miRNAs uncharacterized for MS emerged (miR-15a-3p/124-5p/149-3p/29c-3p/33a-3p/34c-5p/297). PCA showed that distinct miRNA sets segregated MS from controls and relapse from remission. In silico analysis predicted the involvement of these miRNAs in cell cycle, immunoregulation, and neurogenesis, but also revealed that the signaling pathway pattern of remitting MS is more akin to controls rather than patients with relapsing MS.ConclusionsThis study highlights the CSF-predominant dysregulation of miRNAs in MS by identifying a signature of disease activity and intrathecal inflammation among neuroinflammatory disorders.

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Immune-related miRNA expression patterns in peripheral blood mononuclear cells differ in multiple sclerosis relapse and remission

Cited by 50 publications

References 62 publications

Circulating Exosomal miR-17 Inhibits the Induction of Regulatory T Cells via Suppressing TGFBR II Expression in Rheumatoid Arthritis

Circulating Exosomal miR-17 Inhibits the Induction of Regulatory T Cells via Suppressing TGFBR II Expression in Rheumatoid Arthritis

Environmental Influencers, MicroRNA, and Multiple Sclerosis

CSF microRNAs discriminate MS activity and share similarity to other neuroinflammatory disorders

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