Abstract
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.
Highlights
Thyroid-associated ophthalmopathy (TAO) is a sight-threatening orbital disease and the leading type of autoimmune inflammatory disorder of the orbit (Li et al, 2018)
To detect altered methylation status in thyroid-associated ophthalmopathy (TAO) patients compared with normal subjects, orbital adipose/connective tissues of TAO patients (n = 4, age 35.25 ± 6.34, male/female = 1/3) and control subjects (n = 4, age 39.00 ± 7.85, 4 female) were collected
DNA methylation is a stable but modifiable epigenetic process whereby a methyl group is transferred onto the C5 position of a cytosine on DNA sequences and regulates gene expression in response to environmental stimulation
Summary
Thyroid-associated ophthalmopathy (TAO) is a sight-threatening orbital disease and the leading type of autoimmune inflammatory disorder of the orbit (Li et al, 2018). Methylation Analysis of Thyroid-Associated Ophthalmopathy keratitis, corneal ulcers and even compressive optic neuropathy (Bahn, 2010). It cannot be ignored that patients with TAO may experience impaired quality of life and social function, and they could develop neurobehavioral syndrome in the form of anxious to depressive or psychotic disorders (Bruscolini et al, 2018). TAO is recognized as an autoimmune condition mostly associated with Graves’ disease (Bahn, 2010). OF is the critical provider of autoantigens including thyroid stimulating hormone receptor (TSHR) and insulin-like growth factor-1 receptor (IGF-1R), suggesting that it can be both the instigator and main pathological effector of TAO (Smith, 2015). The critical roles of environment and epigenetics in the development of TAO have been emphasized (Yin et al, 2012)
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