Abstract
As part of a systematic investigation of the glycosphingolipids in human tissues, acid and non-acid glycosphingolipids from human thyroid and parathyroid glands were isolated and characterized with mass spectrometry and binding of carbohydrate-recognizing ligands, with a focus on complex compounds. The glycosphingolipid patterns of the human parathyroid and thyroid glands were very similar. The major acid glycosphingolipids were sulfatide and the gangliosides GM3, GD3, GD1a, GD1b, GT1b and Neu5Ac-neolactotetraosylceramide, and the major non-acid glycosphingolipids were globotriaosylceramide and globoside. We also found neolactotetra- and neolactohexaosylceramide, the x2 glycosphingolipid, and complex glycosphingolipids with terminal blood group O and A determinants in both tissues. A glycosphingolipid with blood group Leb determinant was identified in the thyroid gland, and the parathyroid sample had a glycosphingolipid with terminal blood group B determinant. Immunohistochemistry demonstrated the expression of blood group A antigens in both the thyroid and parathyroid glands. A weak cytoplasmatic expression of the GD1a ganglioside was present in the thyroid, while the parathyroid gland had a strong GD1a expression on the cell surface. Thus, the glycosylation of human thyroid and parathyroid glands is more complex than previously appreciated. Our findings provide a platform for further studies of alterations of cell surface glycosphingolipids in thyroid and parathyroid cancers.
Highlights
With an incidence of 1–2%, primary hyperparathyroidism is one of the most prevalent endocrine disorders [1]
Patients with primary hyperparathyroidism may suffer from fatigue, muscle weakness, depression, abdominal discomfort, kidney stones and osteoporosis [2]
Acid and non-acid glycosphingolipids were isolated from parathyroid glands and thyroid glands using standard methods
Summary
With an incidence of 1–2%, primary hyperparathyroidism is one of the most prevalent endocrine disorders [1]. It is caused by the autonomously increased secretion of parathyroid hormone from one or several parathyroid glands. Patients with primary hyperparathyroidism may suffer from fatigue, muscle weakness, depression, abdominal discomfort, kidney stones and osteoporosis [2]. The only curative treatment for primary hyperparathyroidism is surgical removal of all diseased glands. The accuracy of conventional methods, such as parathyroid scintigraphy, ultrasound, and four-dimensional computed tomography (4D-CT), to localize all the diseased glands is limited [3,4].
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