Non-coding RNAs in the Pathogenesis of Multiple Sclerosis

Yousuf, Aadil; Qurashi, Abrar

doi:10.3389/fgene.2021.717922

Cited by 10 publications

(14 citation statements)

References 66 publications

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“…The dysregulation of lncRNAs has been implicated in the causes of various neurological diseases including MS [ 146 ]. LncRNAs play a role in regulating gene expression and controlling immune system responses [ 147 , 148 ]. Several lncRNAs, including MIAT , have been associated with the pathogenesis, prognosis, and diagnosis of MS [ [147] , [148] , [149] , [150] ].…”

Section: Myocardial Infarction Associated Transcript ( Miat...mentioning

confidence: 99%

MIAT LncRNA: A multifunctional key player in non-oncological pathological conditions

Zeinelabdeen,

Abaza,

Yasser

et al. 2024

Non-coding RNA Research

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Section: Myocardial Infarction Associated Transcript ( Miat...mentioning

confidence: 99%

MIAT LncRNA: A multifunctional key player in non-oncological pathological conditions

Zeinelabdeen,

Abaza,

Yasser

et al. 2024

Non-coding RNA Research

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“…Over the past decade, several reports have demonstrated the usefulness of serum RNAs as prognostic and diagnostic biomarkers in various human diseases including MS [ 21 , 22 , 23 ]. Furthermore, the importance of long noncoding RNAs (lncRNAs) in epigenetic regulation of a series of biological processes and their involvement in autoimmune [ 24 ] and inflammatory diseases [ 25 ] have been established.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, the importance of long noncoding RNAs (lncRNAs) in epigenetic regulation of a series of biological processes and their involvement in autoimmune [ 24 ] and inflammatory diseases [ 25 ] have been established. Although many MS-related lncRNAs have been sequenced and their functions have been characterized [ 26 ], and although dysregulated lncRNA expression has been found in serum, plasma, and PBMCs of patients with MS [ 21 ], the expression and the role of several other lncRNAs in MS still remains to be explored.…”

Section: Introductionmentioning

confidence: 99%

Altered Lnc-EGFR, SNHG1, and LincRNA-Cox2 Profiles in Patients with Relapsing-Remitting Multiple Sclerosis: Impact on Disease Activity and Progression

et al. 2023

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Relapsing–remitting multiple sclerosis (RRMS) is the most prevalent MS subtype. Ample evidence has indicated that long noncoding RNAs (lncRNAs) are crucial players in autoimmune and inflammatory disorders. This study investigated the expression of lnc-EGFR, SNHG1, and lincRNA-Cox2 in RRMS patients during active relapses and in remission. Additionally, the expression of FOXP3, a master transcription factor for regulatory T cells, and NLRP3-inflammasome-related genes were determined. Relationships between these parameters and MS activity and annualized relapse rate (ARR) were also evaluated. The study included 100 Egyptian participants: 70 RRMS patients (35 during relapse and 35 in remission) and 30 healthy controls. RRMS patients showed significant downregulation of lnc-EGFR and FOXP3 and dramatic upregulation of SNHG1, lincRNA-Cox2, NLRP3, ASC, and caspase-1 compared to controls. Lower serum TGF-β1 and elevated IL-1β levels were observed in RRMS patients. Notably, patients during relapses displayed more significant alterations than those in remission. Lnc-EGFR was positively correlated with FOXP3 and TGF-β1 and negatively correlated with ARR, SNHG1, lincRNA-Cox2, and NLRP3 inflammasome components. Meanwhile, SNHG1 and lincRNA-Cox2 were positively correlated with ARR, NLRP3, ASC, caspase-1, and IL-1β. Excellent diagnostic performance for lnc-EGFR, FOXP3, and TGF-β1 was demonstrated, while all biomarkers exhibited strong prognostic potential for predicting relapses. Finally, the differential expression of lnc-EGFR, SNHG1, and lincRNA-Cox2 in RRMS patients, especially during relapses, suggests their involvement in RRMS pathogenesis and activity. Correlation between their expression and ARR implies relationships to disease progression. Our findings also highlight their promising roles as biomarkers for RRMS.

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“…Altered ncRNAs can interfere with the correct expression or splicing of specific target genes and can also affect protein functionality 13–15 . In the context of central nervous system autoimmunity, several microRNAs and lncRNAs have been found to be dysregulated in different immune and neuronal cell populations from patients with MS and experimental autoimmune encephalomyelitis models 16,17 …”

Section: Introductionmentioning

confidence: 99%

“…[13][14][15] In the context of central nervous system autoimmunity, several microRNAs and lncRNAs have been found to be dysregulated in different immune and neuronal cell populations from patients with MS and experimental autoimmune encephalomyelitis models. 16,17 Here, we used whole RNA-seq technology to provide the first bona fide description of the ataxin-1-associated ncRNA repertoire in B cells upon an encephalitogenic challenge. Distinct transcriptomic signatures were identified in Atxn1-null mice, with enrichment of processed pseudogenes and intergenic lncRNAs, respectively, at baseline and 10 days after experimental autoimmune encephalomyelitis immunization.…”

Section: Introductionmentioning

confidence: 99%

Ataxin‐1 controls the expression of specific noncoding RNAs in B cells upon autoimmune demyelination

Didonna

2023

Immunol Cell Biol

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B cells play a key mechanistic role in the pathogenesis of multiple sclerosis (MS), a chronic neurological disease of the central nervous system with an autoimmune etiology. B cells contribute to disease initiation and progression by acting as professional antigen-presenting cells as well as via secreting autoantibodies and proinflammatory cytokines. We have recently shown that the polyglutamine protein ataxin-1, which was first linked to the movement disorder spinocerebellar ataxia type 1, also acts as a master regulator of B-cell functions in the context of central nervous system autoimmunity. In fact, ataxin-1-deficient mice display an aggravated manifestation of the MS disease model experimental autoimmune encephalomyelitis along with aberrant B-cell functions. Consistent with this scenario, transcriptomic analysis of Atxn1-null B cells highlighted distinct genetic signatures involved in cell activation, proliferation and antigen presentation. To further characterize the role of ataxin-1, we profiled the noncoding transcriptome controlled by ataxin-1 in the B-cell compartment upon an encephalitogenic challenge. We show that two specific classes of noncoding RNAs, namely, processed pseudogenes and intergenic long noncoding RNAs, are differentially regulated along disease. Furthermore, pathway and protein network analyses on their putative proteincoding gene targets found a significant enrichment in ontologies related to cell mitosis, together with molecular processes relevant to MS such as chitin metabolism. Altogether, these findings shed light on the possible contribution of noncoding RNAs to B-cell biology and MS pathogenesis, and further establish the immunomodulatory role of ataxin-1 in autoimmune demyelination.

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Non-coding RNAs in the Pathogenesis of Multiple Sclerosis

Cited by 10 publications

References 66 publications

MIAT LncRNA: A multifunctional key player in non-oncological pathological conditions

MIAT LncRNA: A multifunctional key player in non-oncological pathological conditions

Altered Lnc-EGFR, SNHG1, and LincRNA-Cox2 Profiles in Patients with Relapsing-Remitting Multiple Sclerosis: Impact on Disease Activity and Progression

Ataxin‐1 controls the expression of specific noncoding RNAs in B cells upon autoimmune demyelination

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