Calsequestrin is Decreased in the Thyroid Gland of Patients with Graves’ Disease – Further Evidence for a Role of Autoimmunity against this Protein in Graves’ Ophthalmopathy.
Western blotanalysis showed the presence of two forms of CASQ1 in the thyroid, of 50 and 60 kDa molecular weight respectively. In thyroidtissues, the mean (± SD) (GO 54.9±86.8 pmol/mg) concentration of the CASQ1 protein (GH 37.1±51.8 pmol/mg) was significantly reduced in patients with Graves’ disease , with or without ophthalmopathy, compared to normal thyroidtissues from control subjects with multinodular goitre or thyroid cancer (144.3±162.5 pmol/mg). The difference between GO and GH was not significant. The decreased CASQ1 protein levels in Graves’ thyroidtissues correlated with the homozygous genotype of the rs3838216 CASQ1 polymorphism. A two-fold increase in Levels of CASQ1 protein in toxic nodules compared to Graves’ hyperthyroidism was markedly significant.
Conclusions:
Decreased CASQ1 in the thyroidtissues of patients with Graves’ disease compared to normal thyroidtissues from control subjects may reflect consumption of the protein in the course of an autoimmune reaction against CASQ1 in the thyroid. Comparing CASQ1 protein levels in thyroidtissue from five patients with toxic nodular goitre (74.5±52.8) to controls showed no significance. The relative two fold increase in CASQ1 levels in toxic nodules compared to Graves’ disease suggests that this is due to the autoimmune reaction rather than the hyperthyroidism.