MicroRNAs and Autoimmune-Mediated Eye Diseases

Wei, Yankai; Li, Na; Zhao, Lu; Yang, Chao; Ma, Binyun; Li, Xiaorong; Wei, Ruihua; Nian, Hong

doi:10.3389/fcell.2020.00818

Cited by 26 publications

(21 citation statements)

References 96 publications

(102 reference statements)

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“…In addition, miRNAs could also bind the 5'UTR region and the promoter region, inducing translational activation [9]. A key role of microRNAs in the regulation of the immune response has been highlighted, so it is not surprising that aberrant expression of miRNAs has been demonstrated in numerous autoimmune diseases [10,11], included SS.…”

Section: Introductionmentioning

confidence: 99%

Emerging Role of microRNAs and Long Non-Coding RNAs in Sjögren’s Syndrome

Benedittis

Ciccacci

Latini

et al. 2021

Genes

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Sjögren’s Syndrome (SS) is a chronic autoimmune inflammatory disease. It is considered a multifactorial pathology, in which underlying genetic predisposition, epigenetic mechanisms and environmental factors contribute to development. The epigenetic regulations represent a link between genetic predisposition and environmental factors. Recent studies suggested a regulatory role for non-coding RNAs in critical biological and disease processes. Among non-coding RNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) play a critical role in the post-transcriptional mRNA expression, forming a complex network of gene expression regulation. This review aims to give an overview of the latest studies that have investigated the role of miRNAs and lncRNAs in the SS. We included papers that investigated the expression of non-coding RNAs on different tissues, in particular on peripheral blood mononuclear cells and salivary glands. However, regarding the involvement of non-coding RNAs genetic variability in SS susceptibility very few data are available. Further research could help to elucidate underlying pathogenic processes of SS and provide new opportunities for the development of targeted therapies.

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Section: Introductionmentioning

confidence: 99%

Emerging Role of microRNAs and Long Non-Coding RNAs in Sjögren’s Syndrome

Benedittis

Ciccacci

Latini

et al. 2021

Genes

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“… 4 , 36 The exact mechanism in the progression of TAO is unclear although several studies implicate TSHR and IGF-1R, which are both upregulated in the OFs of patients with TAO. 5 , 37 The miRNA regulation of genes involved in TAO is gaining interest, 38 therefore, in our study, we focused on miRNA that may be involved in the regulation of the inflammasome in TAO using relevant markers such as NLRP3. We found a number of miRNAs that were differentially regulated in the orbital connective tissue of TAO patients and confirmed that three of these were significantly upregulated (miR-22, miR-27b, and miR-378) and one was significantly downregulated (miR-143).…”

Section: Discussionmentioning

confidence: 99%

MiR-143 Targets IGF-1R to Suppress Autoimmunity in Thyroid-Associated Ophthalmopathy

Tang¹,

Liu²,

Huang³

et al. 2022

JIR

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Objective Thyroid-associated ophthalmopathy (TAO) is an autoimmune disease that involves the remodeling of orbit and periorbital tissues. Thyroid-stimulating hormone receptor (TSHR) and insulin-like growth factor 1 receptor (IGF-1R) may stimulate the activation of autoimmunity in TAO, but the exact mechanism is unclear. We investigated whether IGF-1R/TSHR modulation in TAO may involve microRNA regulation. Methods We conducted microarray analysis using RNA from the orbital connective tissue samples of 3 healthy and 3 patients with TAO. The involvement of differentially regulated microRNA in IGF-1R/TSHR modulation in TAO was evaluated in orbital fibroblasts (OFs) and female BALB/c mice. Results Using hierarchical cluster analysis, we identified that miR-143 was downregulated in TAO. The expression levels of miR-143 in OFs were significantly reduced under IL-1B stimulation. However, OF proliferation and inflammatory responses decreased when miR-143 is overexpressed. In contrast, the suppression of miR-143 increased levels of inflammatory markers (IL-6, IL-8, MCP1) and hyaluronan accumulation. Moreover, overexpression of miR-143 significantly lowers levels of IGF-1R and TSHR. A luciferase assay indicated that miR-143 targets the 3′-UTR of IGF-1R. Increases in the expression of IGF-1R increased the expression of the inflammasome marker NLRP3 and apoptotic marker cleaved caspase-1; however, miR-143 overexpression decreased levels of IGF-1R, TSHR, NLRP3, cleaved caspase 1, IL-1B, and IL-18. In a mouse model of TAO, overexpression of miR-143 significantly reduced levels of IGF-1R and attenuated the adipogenesis associated with TAO. Conclusion We found that miR-143 directly targets IGF-1R to alleviate the inflammatory response in TAO by indirectly decreasing levels of TSHR and inactivating NLRP3.

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“…MiRNAs can regulate more than 60% of protein- coding genes in the humans and have been implicated in the various biological processes such as the lineage commitment in the immune system, cell proliferation, differentiation, apoptosis, and maintenance of immune homeostasis ( 56 , 57 ). An abnormal expression of miRNAs has been closely related to the pathogenesis of various autoimmune-mediated eye diseases such as GO ( 58 ). Circulating miRNAs can be detected in the peripheral blood and orbital tissues of GO patients, with different expression levels in the active disease stage of GO.…”

Section: Non-coding Rnas and Gomentioning

confidence: 99%

Emerging Insights Into the Role of Epigenetics and Gut Microbiome in the Pathogenesis of Graves’ Ophthalmopathy

Wang

et al. 2022

Front. Endocrinol.

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Graves’ Ophthalmopathy (GO) is an organ-specific autoimmune disease that is often characterized by infiltration of orbital tissues and is considered as the most common extra-thyroid manifestation of Graves’ disease (GD). Although genetic susceptibility has been found to be critical for the phenotype of GO, the associated risk alleles in a single gene are generally insufficient to cause the disease. Accruing evidence has shown that epigenetic disorders can act as the potentially missing link between genetic risk and clinically significant disease development. Abnormal epigenetic modifications can lead to pro-inflammatory cascades and activation of orbital fibroblasts (OFs) by promoting the various inflammatory response pathways and regulating the diverse signaling molecules that are involved in the fibrogenesis and adipogenesis, thereby leading to the significant expansion of orbital tissues, fibrosis and inflammation infiltration. Additionally, emerging evidence has shown that the gut microbiome can possibly drive the pathogenesis of GO by influencing the secretion of Thyrotropin receptor antibody (TRAb) and T-helper 17 (Th17)/regulatory T cells (Treg) imbalance. This paper describes the latest epigenetic research evidence and progress made in comprehending the mechanisms of GO development, such as DNA methylation, histone modification, non-coding RNAs, and the gut microbiome.

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MicroRNAs and Autoimmune-Mediated Eye Diseases

Cited by 26 publications

References 96 publications

Emerging Role of microRNAs and Long Non-Coding RNAs in Sjögren’s Syndrome

Emerging Role of microRNAs and Long Non-Coding RNAs in Sjögren’s Syndrome

MiR-143 Targets IGF-1R to Suppress Autoimmunity in Thyroid-Associated Ophthalmopathy

Emerging Insights Into the Role of Epigenetics and Gut Microbiome in the Pathogenesis of Graves’ Ophthalmopathy

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