Identification of differentially expressed long non-coding RNAs and mRNAs in orbital adipose/connective tissue of thyroid-associated ophthalmopathy

Wu, Lianqun; Li, Lei; Chen, Xinxin; Mou, Pei; Li, Guohua; Sun, Xiantao; Qin, Bing; Zhang, Shujie; Zhao, Chen

doi:10.1016/j.ygeno.2020.09.001

Cited by 13 publications

(16 citation statements)

References 48 publications

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“…The genetic and immune factors of TAO and anti-immune therapy are receiving increasing clinical attention and are being studied more and more. Previous studies on the mechanisms of TAO have focused on orbital adipose tissue and extraocular muscles, but little research has been conducted on the lacrimal gland (11)(12)(13). In this study, 15 irDEGs, represented by JAK1, HSP90AA1, PLA2G2A, FGF3, GPI, and PDIA2, were screened by a differential analysis of TAO genes and normal human lacrimal gland expressed genes, and the intersecting immune genes were identified.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of immune-related differentially expressed genes in thyroid-associated ophthalmopathy based on the GEO database

Gao¹,

Li²

2022

Ann Transl Med

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Background We performed a differential analysis, enrichment analysis, and immune-infiltration analysis of the thyroid-associated ophthalmopathy (TAO) gene using data from the Gene Expression Omnibus (GEO) database to provide a theoretical basis for understanding the immune-related mechanisms of TAO. Methods We searched the GEO database for “Graves disease” and selected the genes expressed in the lacrimal gland of thyroid-related eye disease patients as the test group and the genes expressed in the lacrimal gland of normal subjects as the control group. Immune-related differentially expressed genes (irDEGs), gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, protein-protein interaction, gene-gene interaction (GGI) network, pivotal gene identification, and immune-infiltration analyses were carried out, and finally, risk-prediction models were constructed. Results The GSE105149 and GSE58331 data sets contained 200 DEGs, of which 15 were immune-related. In relation to the GO biological processes (BPs), the main pathways included the interleukin (IL)-27-mediated signaling pathway, the IL-35-mediated signaling pathway, cytokine activity, T helper 17 cell differentiation, the phosphatidylinositol-3-kinase and protein kinase B signaling pathway, cytokine-cytokine receptor interaction, the Janus kinase and signal transducer and activator of transcription signaling pathway, and other KEGG pathways. Cluster of differentiation (CD)4 + T cells, monocytes, M0 macrophages, and Mast cells were significantly elevated in TAO, while M2 macrophages were significantly reduced. In the immune cell correlation analysis, CD4 + T cells and naïve B cells were significantly positively correlated with activated natural killer (NK) cells, and Mast cells were positively correlated with plasma cells and negatively correlated with M2 macrophages. Risk models for a total of 6 genes (i.e., Janus kinase 1, heat shock protein 90-α, phospholipase A 2 group IIA, fibroblast growth factor 3, glucose-6-phosphate isomerase, and protein disulfide isomerase family A, member 2), were constructed, and over 100 potential targeted therapeutic agents were obtained. Conclusions In TAO, various types of immune cells infiltrate to different degrees, and the immune response and inflammatory response are throughout the disease. Our constructed risk-prediction models provide a reference for predicting TAO.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of immune-related differentially expressed genes in thyroid-associated ophthalmopathy based on the GEO database

Gao¹,

Li²

2022

Ann Transl Med

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“…We have performed gene expression analysis in TAO patients in previous article ( Wu et al, 2021 ). Methylation analysis and expression analysis shared several identical results in GO terms and KEGG pathways.…”

Section: Discussionmentioning

confidence: 99%

Adipose/Connective Tissue From Thyroid-Associated Ophthalmopathy Uncovers Interdependence Between Methylation and Disease Pathogenesis: A Genome-Wide Methylation Analysis

Ding

Wang

et al. 2021

Front. Cell Dev. Biol.

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In response to pathological stimulation, methylation status conversion of the genome drives changes of cell feature and is able to promote disease development. Yet the role of methylation in the development of thyroid-associated ophthalmopathy (TAO) remains to be evaluated. Overexpansion of orbital tissue is the key feature of TAO. In this study, the methylation profile of orbital adipose/connective tissue from TAO patients and normal individuals were compared. After screening 3,739 differentially methylated probes, the distribution and properties of these probes were analyzed. Furthermore, enriched biological functions of these genes associated with differential methylation and the relationship between their methylation status and expression profile were also identified, including PTPRU and VCAM-1. According to our results, methylation was involved in disregulated immune response and inflammation in TAO and might contribute to activation of fibroblast and adipogenesis, leading to the expansion of orbital tissue. Neuropathy and neurobehavioral symptoms were also potentially associated with methylation. These results may help to extend the understanding of methylation in TAO and provide more insights into diagnosis and treatment of patients.

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“…found that co-expression interactions between differentially expressed lncRNAs and 52 ECM-related mRNAs (e.g., COL12A1, TNXB, COL6A3, KAZALD1, FBN1 and SPON1) in GO patients’ orbital adipose/connective tissue samples suggest that lncRNAs may regulate ECM function in GO patients’ orbital adipose/connective tissue from ( 89 ). For example, co-expression interactions of lncRNA with COL12A1 and negative co-expression of lnc-PTP4A2-3:7 with TNXB may be associated with altered ECM in GO orbital adipose/connective tissue ( 89 ). Wang et al.…”

Section: Non-coding Rnamentioning

confidence: 99%

Research progress on the pathogenesis of Graves’ ophthalmopathy: Based on immunity, noncoding RNA and exosomes

et al. 2022

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Graves’ ophthalmopathy (GO), also known as thyroid-associated ophthalmopathy, is a common potentially vision-threatening organ-specific autoimmune disease and the most common extrathyroidal manifestation of Graves’ disease. It can happen to those who have hyperthyroidism or euthyroidism. At present, the pathogenesis of GO has not been fully elucidated, and the majority of clinical treatments are symptomatic. Therefore, we are eager to discover any new therapeutic strategies that target the etiology of GO. To provide fresh ideas for the creation of new therapeutic techniques, this study primarily discusses the research state and progress of GO-related pathogenesis from the perspectives of GO’s cellular immunity, autoantigens, non-coding RNAs, and exosomes.

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Identification of differentially expressed long non-coding RNAs and mRNAs in orbital adipose/connective tissue of thyroid-associated ophthalmopathy

Cited by 13 publications

References 48 publications

Mechanisms of immune-related differentially expressed genes in thyroid-associated ophthalmopathy based on the GEO database

Mechanisms of immune-related differentially expressed genes in thyroid-associated ophthalmopathy based on the GEO database

Adipose/Connective Tissue From Thyroid-Associated Ophthalmopathy Uncovers Interdependence Between Methylation and Disease Pathogenesis: A Genome-Wide Methylation Analysis

Research progress on the pathogenesis of Graves’ ophthalmopathy: Based on immunity, noncoding RNA and exosomes

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