LncRNAs in adaptive immunity: role in physiological and pathological conditions

Zeni, Pedro Faria; Mráz, Marek

doi:10.1080/15476286.2020.1838783

Cited by 34 publications

(20 citation statements)

References 155 publications

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“…Recent research suggests that some lncRNAs can encode peptides, which act as crucial pathogenic agents of many diseases [173]. Additionally, lncRNAs play an important role in immune response and are involved in autoimmune disease development [174]. As a full-scale characterisation of lncRNAs is far beyond the scope of this review, we wish to redirect interested readers to the cited papers for further information.…”

Section: Long Noncoding Rnas-new Regulators Of Pcos Inflammationmentioning

confidence: 99%

Mitochondrial Dysfunction and Chronic Inflammation in Polycystic Ovary Syndrome

Dabravolski

Nikiforov

Eid

et al. 2021

IJMS

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Polycystic ovarian syndrome (PCOS) is the most common endocrine–metabolic disorder affecting a vast population worldwide; it is linked with anovulation, mitochondrial dysfunctions and hormonal disbalance. Mutations in mtDNA have been identified in PCOS patients and likely play an important role in PCOS aetiology and pathogenesis; however, their causative role in PCOS development requires further investigation. As a low-grade chronic inflammation disease, PCOS patients have permanently elevated levels of inflammatory markers (TNF-α, CRP, IL-6, IL-8, IL-18). In this review, we summarise recent data regarding the role of mtDNA mutations and mitochondrial malfunctions in PCOS pathogenesis. Furthermore, we discuss recent papers dedicated to the identification of novel biomarkers for early PCOS diagnosis. Finally, traditional and new mitochondria-targeted treatments are discussed. This review intends to emphasise the key role of oxidative stress and chronic inflammation in PCOS pathogenesis; however, the exact molecular mechanism is mostly unknown and requires further investigation.

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Section: Long Noncoding Rnas-new Regulators Of Pcos Inflammationmentioning

confidence: 99%

Mitochondrial Dysfunction and Chronic Inflammation in Polycystic Ovary Syndrome

Dabravolski

Nikiforov

Eid

et al. 2021

IJMS

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“…Note that the genomic positions of lncRNAs are of a special importance. Many lncRNAs reside in chromosomal locations that overlap with miRNAs, suggesting that such lncRNAs may act as splicing regulators or antisense (i.e., competing with the gene where it resides in) [64]. For example, miR-3128 is found in the intron of NFE2L2 that encodes the Nrf2 transcription factor (TF).…”

Section: Discussionmentioning

confidence: 99%

Alteration in Long Noncoding RNAs in Response to Oxidative Stress and Ladostigil in SH-SY5Y Cells

Zohar¹,

Giladi²,

Eliyahu³

et al. 2022

Preprint

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Microglia activation causes neuroinflammation, which is a hallmark of neurodegenerative disorders, brain injury, and aging. Ladostigil, a bifunctional reagent with antioxidant and anti-inflammatory properties, reduced microglial activation and enhanced brain functioning in elderly rats. In this study, we studied SH-SY5Y, a human neuroblastoma cell line, and tested viability in the presence of hydrogen peroxide and Sin1 (3-morpholinosydnonimine), which generates reactive oxygen and nitrogen species (ROS/RNS). Both stressors caused significant apoptosis and necrotic cell death that was attenuated by ladostigil. Our results from RNA-seq experiments show that long non-coding RNAs (lncRNAs) account for 30% of all transcripts in SH-SY5Y cells treated with Sin1 for 24 hours. Altogether, we identify 94 differently expressed lncRNAs in the presence of Sin1, including MALAT1, a highly expressed lncRNA with anti-inflammatory and anti-apoptotic functions. Additional activities of Sin-1 upregulated lncRNAs include redox homeostasis (e.g., MIAT, GABPB1-AS1), energy metabolism (HAND2-AS1), and neurodegeneration (e.g., MIAT, GABPB1-AS1, NEAT1). Four lncRNAs implicated as enhancers were significantly upregulated in cells exposed to Sin1 and ladostigil. Finally, we show that H2O2 and Sin1 increased the expression of DJ-1, a redox sensor and modulator of Nrf2 (nuclear factor erythroid 2–related factor 2). Nrf2 (NFE2L2 gene) is a major transcription factor regulating antioxidant genes. In the presence of ladostigil, DJ-1 expression is restored to its baseline. The mechanisms governing SH-SY5Y cell survival and homeostasis are highlighted by the beneficial role of ladostigil in the crosstalk involving Nrf2, antioxidant transcription factor DJ-1, and lncRNAs. Stress-dependent induction of lncRNAs represents an underappreciated regulatory level that contributes to cellular homeostasis and the capacity of SH-SY5Y to cope with oxidative stress.

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“…The plasmacytoma variant translocation oncogene ( PVT1 ) is located in the 8q24.21 region, which is a preferred site for chromosomal rearrangements in cancers and incorporates multiple risk loci for MS [ 70 , 71 ]. The lymphocyte activation through the involvement of PVT1 is implicated in adaptive immunity and has implications for autoimmune diseases (MS, inflammatory bowel disease, rheumatoid arthritis) [ 72 , 73 ]. In a study involving 296 RRMS patients (from Russia) treated with GA, the A allele of the rs2114358 (A > G; intron variant) polymorphism was associated with event-free status ( Table 1 ) [ 57 ].…”

Section: Pharmacogenetics Of Glatiramer Acetate In Msmentioning

confidence: 99%

Influence of Genetic Polymorphisms on Clinical Outcomes of Glatiramer Acetate in Multiple Sclerosis Patients

Zarzuelo

Pérez-Ramírez

Cura

et al. 2021

JPM

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Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of autoimmune origin, in which inflammation and demyelination lead to neurodegeneration and progressive disability. Treatment is aimed at slowing down the course of the disease and mitigating its symptoms. One of the first-line treatments used in patients with MS is glatiramer acetate (GA). However, in clinical practice, a response rate of between 30% and 55% is observed. This variability in the effectiveness of the medication may be influenced by genetic factors such as polymorphisms in the genes involved in the pathogenesis of MS. Therefore, this review assesses the impact of genetic variants on the response to GA therapy in patients diagnosed with MS. The results suggest that a relationship exists between the effectiveness of the treatment with GA and the presence of polymorphisms in the following genes: CD86, CLEC16A, CTSS, EOMES, MBP, FAS, TRBC1, IL1R1, IL12RB2, IL22RA2, PTPRT, PVT1, ALOX5AP, MAGI2, ZAK, RFPL3, UVRAG, SLC1A4, and HLA-DRB1*1501. Consequently, the identification of polymorphisms in these genes can be used in the future as a predictive marker of the response to GA treatment in patients diagnosed with MS. Nevertheless, there is a lack of evidence for this and more validation studies need to be conducted to apply this information to clinical practice.

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LncRNAs in adaptive immunity: role in physiological and pathological conditions

Cited by 34 publications

References 155 publications

Mitochondrial Dysfunction and Chronic Inflammation in Polycystic Ovary Syndrome

Mitochondrial Dysfunction and Chronic Inflammation in Polycystic Ovary Syndrome

Alteration in Long Noncoding RNAs in Response to Oxidative Stress and Ladostigil in SH-SY5Y Cells

Influence of Genetic Polymorphisms on Clinical Outcomes of Glatiramer Acetate in Multiple Sclerosis Patients

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