Abstract
Graves' ophthalmopathy (GO) is a chronic autoimmune inflammatory disorder involving orbital tissues. A receptor for advanced glycation end products (RAGE) and its ligand high mobility group box 1 (HMGB1) protein trigger inflammation and cell proliferation and are involved in the pathogenesis of various chronic inflammatory diseases. This study was aimed to evaluate RAGE and HMGB1 expression in GO to determine its potential clinical significance. To the best of our knowledge, this is the first study showing RAGE and HMGB1 expression in orbital tissue using immunohistochemistry. Sections of orbital adipose tissue obtained from patients diagnosed with GO (23 patients; 36 orbits) and normal controls (NC) (15 patients; 15 orbits) were analyzed by immunohistochemistry for RAGE and HMGB1 expression. Expression profiles were then correlated with clinical data of the study group. RAGE and HMGB1 expression were elevated in GO patients in comparison with NC (p = 0.001 and p = 0.02, respectively). We observed a correlation between RAGE expression and occurrence of dysthyroid optic neuropathy (DON) (p = 0.05) and levels of TSH Receptor Antibodies (TRAb) (p = 0.01). Overexpression of RAGE and HMGB1 might be associated with GO pathogenesis. In addition, RAGE and HMGB1 proteins may be considered as promising therapeutic targets, but this requires further research.
Highlights
Graves’ disease (GD) represents an autoimmune process in which circulating autoantibodies directed against thyrotropin receptor (TSHR)—TSH Receptor Antibodies (TRAb) (TSHR antibodies)—activate the thyroid gland, causing hyperthyroidism [1]
receptor for advanced glycation end products (RAGE) expression levels were elevated in Graves’ ophthalmopathy (GO) tissues compared to those from normal controls (NC) (p = 0:001; Figure 1(a))
high mobility group box 1 (HMGB1) was detectable in the nuclei and cytoplasm in all tissues of GO patients and NC (Figure 1(b))
Summary
Graves’ disease (GD) represents an autoimmune process in which circulating autoantibodies directed against thyrotropin receptor (TSHR)—TRAb (TSHR antibodies)—activate the thyroid gland, causing hyperthyroidism [1]. One of the extrathyroidal symptoms of GD is Graves’ ophthalmopathy (GO), defined as a chronic autoimmune inflammatory disorder involving orbital tissues [2]. Patients with GO are mostly hyperthyroid, they can be euthyroid or hypothyroid. GO may be reported in Hashimoto’s thyroiditis [3]. Inflammatory infiltration, and orbital fibroblast activity result in expansion and remodeling of extraocular tissues—mainly orbital adipose tissue and fibrous tissue of extraocular muscles. Edematousinfiltrative changes involving orbital soft tissues are observed
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