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High levels of DNA polymerase β mRNA corresponding with the high activity in Graves' thyroid tissue.

AbstractINTRODUCTION:
High DNA polymerase β activity has been observed in the thyroid tissue of patients with Graves' disease (Nagasaka et al. in Metabolism 37:1051-1054, 1988). This fact aroused our interest in whether the alteration of DNA polymerase β activity depends on DNA polymerase β (DNA poly β) mRNA levels, which may be modulated by thyroid-stimulating hormone (TSH) or thyroid-stimulating substances, i.e. TSH receptor antibody (TRAb).
RESULT:
Addition of TSH or TRAb to primary cultures of Graves' disease thyroid cells for 4 h led to no increase in DNA poly β mRNA levels. In contrast, thyroid hormone synthesizing enzyme, peroxidase, mRNA levels increased fivefold after coculture with TSH and TRAb, even though DNA poly β activity and mRNA levels are already significantly higher in Graves' disease thyroid tissues, compared with normal thyroid tissue.
DISCUSSION:
These results indicate that DNA poly β expression in Graves' disease thyroid cells may be maximally activated or plateau in response to thyroid-stimulating immunoglobulins, or that the activation of to poly β expression may occur via pathways other than the G protein and cyclic AMP system.
AuthorsN Hayakawa, Y Sato, A Nagasaka, Y Mano, T Nagasaka, A Nakai, K Iwase, S Yoshida
JournalJournal of endocrinological investigation (J Endocrinol Invest) Vol. 40 Issue 4 Pg. 385-389 (Apr 2017) ISSN: 1720-8386 [Electronic] Italy
PMID27848228 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Autoantigens
  • Immunoglobulins, Thyroid-Stimulating
  • Iron-Binding Proteins
  • RNA, Messenger
  • Receptors, Thyrotropin
  • Thyroid Hormones
  • Thyrotropin
  • TPO protein, human
  • Iodide Peroxidase
  • DNA Polymerase beta
Topics
  • Autoantigens (genetics)
  • Blotting, Northern
  • Cells, Cultured
  • DNA Polymerase beta (genetics)
  • Graves Disease (enzymology, genetics, pathology)
  • Humans
  • Immunoglobulins, Thyroid-Stimulating (pharmacology)
  • Iodide Peroxidase (genetics)
  • Iron-Binding Proteins (genetics)
  • RNA, Messenger (genetics)
  • Receptors, Thyrotropin (immunology)
  • Thyroid Gland (enzymology, pathology)
  • Thyroid Hormones (metabolism)
  • Thyrotropin (pharmacology)

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